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ABSTRACT: Cocaine (COC) has been reported to cause effects similar to physiological stressors in the brain neuroendocrinal system, including heat-shock protein (HSP) expression, although these effects have not been elucidated in detail. In the present study, we examined the effects of repeated (4 days) treatments with cocaine hydrochloride (35 mg/kg, i.p.) and 10 min immobilization stress (IM) on the distribution of HSP (HSP27, HSP60, HSP70, HSC70) and stress-activated protein kinase (SAPK) (SAPKalpha, SAPKbeta, SAPKgamma) immunoreactive nerve cells (positive cells) in the rat hippocampus. The swimming behaviors of the rats in the forced swimming test were also examined. In both COC and IM groups, an early enhancement (5 h time point) of hippocampal HSP (HSP27, HSP60, HSP70, HSC70) and SAPK (SAPKbeta, SAPKgamma) positive cells was observed, whereas a recovery (SAPKs) or attenuation (HSP60 and HSC70) was observed at the 24 h time point. In both groups, a depression of the swimming behaviors (attenuation in the activity counts and time until immobility) below the control level was observed at the 5 h point, but a recovery was observed at the 24 h time point. At the 48 h time point, all parameters returned to the control level. These alterations in the levels of HSPs and SAPKs, and the swimming behaviors were similar to those observed in the stress (IM) group, and were characteristic in that all of these alterations were attenuated by the benzodiazepine inverse agonist, Ro 15-4513 (5 mg/kg, i.p.), and the dopamine D1 receptor antagonist, SCH23390 (0.5 mg/kg, i.p.), which was not observed in the groups treated with another stressor-like drug (bicuculline).
Behavioural Pharmacology 12/2003; 14(7):551-62. · 2.72 Impact Factor
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ABSTRACT: To investigate the pathogenetic mechanisms of brain maldevelopment induced by maternal hyperthermia, we exposed pregnant ICR mice to 43 degrees C for 12.5 min on day 13.5 or 14.5 of gestation and examined the proliferation and migration of neuronal precursor cells in the telencephalon of their fetuses. The brain weight was significantly decreased in heat-stressed fetuses when examined at 72 h after treatment. Histological examination revealed that the thickness of the neopallium, especially that of the intermediate (migratory) zone and the cortical plate, was decreased in the heated group. BrdU/anti-BrdU immunohistochemistry showed that cell proliferation in the matrix cell zone was suppressed for up to 8 h after hyperthermia and that the migration of BrdU-labeled neurons from the matrix cell zone to the primordial cortex was decelerated significantly. In addition, apoptotic cell death which is rarely observed in the brain of control animals increased in the brain of heat-stressed fetuses at 8-12 h after treatment. Thus, it seems that brief hyperthermia at critical stages of neuronal differentiation can interfere with the production and migration of neuronal precursor cells and result in abnormal brain development and neurobehavioural disturbances.
Developmental Brain Research 01/2002; 132(1):59-67. · 1.78 Impact Factor
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Ryōikibetsu shōkōgun shirīzu. 02/2001;
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Ryōikibetsu shōkōgun shirīzu. 02/2001;
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ABSTRACT: The ontogenesis of two anti-oxidative enzymes, thioredoxin (TRX) and glutaredoxin (GRX), was examined immunohistochemically in mouse embryos and fetuses at various developmental stages. They were found to be localized in various tissues, with some tissue specificity and temporal sequence. Both TRX and GRX began to be expressed in many tissues at embryonic (E) day E10 or E11 and tended to increase as the developmental stage advanced. In the heart and neuroepithelium, however, their immunoreactivity was already positive at E8.5. In some fetal organs like the liver, pancreas and kidney, TRX and GRX showed heterogeneous localization, suggesting that their expression may reflect the variable functional states of the cell. These results suggest that TRX and GRX may be associated with tissue differentiation in embryos and fetuses are involved in the acquisition of the capacity of resistance against oxygen radicals.
Italian journal of anatomy and embryology = Archivio italiano di anatomia ed embriologia 02/2001; 106(2 Suppl 2):137-42.
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ABSTRACT: It has been shown that branching morphogenesis of the lung bud is mediated by epithelial-mesenchymal interaction via such molecules as FGF10, BMP4 and Shh. However, a recent study showed that the isolated lung epithelium still undergoes branching morphogenesis in vitro even in the absence of mesenchyme (Nogawa and Ito, 1995). In the present study, we observed in vitro the dynamic movement of the isolated lung epithelium of the fetal mouse using time-lapse recording, and investigatedthe roles of actinfilaments in branching of the lung bud. First, time-lapse observation of the initial phase of lung branching morphogenesis revealed that at the sites of cleft formation, the epithelial surface was retracted inward from its original position. From this observation we assumed that there should be some structures which exert a physical force on the epithelium, and the localization and arrangement of actin fibers in the cultured lung epithelium were examined at various stages of branching morphogenesis. At the prebudding (6 h) and onset-budding (24 h) stages, no specific localization of actin filaments was observed in the lung bud epithelium, but at the postbudding stage (48 h) they were localized densely in the cells at the tip of the branched lung epithelium. The cell density was not different between the tip and cleft regions of the lung bud epithelium. When cultured with FGF-soaked beads, an actin-rich region was induced at the tip of the lung bud which was growing toward an FGF-soaked bead. These results indicate that actin fibers do not play a significant part in cleft formation but can be secondarily induced by FGF in the surrounding matrix and play some roles at later shaping of the branch in lung morphogenesis.
The International Journal of Developmental Biology 01/2001; 44(8):899-902. · 2.82 Impact Factor
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ABSTRACT: Mouse newborns find their mother's nipples and suckle milk by themselves. It has been argued which sense organ they use when locating their mother's nipples to suckle milk. Olfactory or tactile sensory systems are primary candidates. In the present study, we investigated the trigeminal-whisker sensory and olfactory systems in genetic arhinencephaly mouse embryos (Pdn/Pdn). Pdn/Pdn newborns do not suckle milk and die within 1 day after birth. Dysfunction of nipple-searching behavior was clear in Pdn/Pdn newborns. Pdn/Pdn newborns had a complete developmental failure in the olfactory nerve projection to the central nervous system and no olfactory bulb architecture. The trigeminal-whisker system was intact in this strain. From the results of these experiments, it was suggested that the olfactory system is essential for nipple-searching behavior and suckling milk and that the trigeminal-whisker system is not able to substitute for the lack of olfactory input in mouse newborns.
Biology of the Neonate 12/2000; 78(4):293-9. · 1.90 Impact Factor
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ABSTRACT: The purpose of the present work was to determine the effects of the hereditary malformation of Hammertoe mutant mice (gene symbol Hm) on the surrounding morphological structures and, specifically, on the volar pads, i.e., the sites of the epidermal ridge patterns (dermatoglyphics). The hindlimbs of the wild-type (+/+) Hammertoe mice show no anomalies and their major pad and flexion crease configurations correspond to those of normal mice. The heterozygous (Hm/+) and homozygous (Hm/Hm) mice display a fusion of the interdigital tissues involving all digits with the exception of digit I. In Hm/Hm mice, this webbing extends to the distal phalanx and the markedly flexed digits form a shape resembling a hammer. In Hm/+ mice, the interdigital webbing does not extend as far and the digits show moderate flexion compared to those of Hm/Hm mice. Both Hm/Hm and Hm/+ have a rudimentary extra digit in the postaxial area of the hindlimbs. The ventral volar skin of the flexed digits is incompletely developed. The more posterior digits show the more severe camptodactyly. These aberrant configurations are related to the abnormal occurrence of the programmed cell death (PCD) in the interdigital zones II-IV and the proximal part of the postaxial margin during hindlimb development. They are limited to the pads on the plantar surface of the postaxial area; the preaxial area is not affected. As a result of a severe camptodactyly of digit V, its volar skin is shifted into the distal portion of the hypothenar area. This shifting affects the number, size, and location of the pads, especially of the hypothenar pad, resulting in varying pad configurations, such as a displacement of the distal and proximal components of the hypothenar pad, or a fusion of the two components of the hypothenar pad, leading to a reduced final pad number. These pad modifications are induced by the postaxial plantar surface shifting proximally and are not affected by the presence of an extra rudimentary digit. The pad modifications in Hammertoe mice with webbed digits and postaxial polydactyly resemble closely those of the previously studied mice with genetic preaxial polydactyly.
The Anatomical Record 10/2000; 260(1):26-32.
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ABSTRACT: The closure of the neural tube (NT) in the human embryo has generally been described as a continuous process that begins at the level of the future cervical region and proceeds both rostrally and caudally. On the other hand, multiple initiation sites of NT closure have been demonstrated in mice and other animals. In humans, based on the study of neural tube defects (NTD) in clinical cases, van Allen et al. (1993) proposed a multisite NT closure model in which five closure sites exist in the NT of human embryos. In the present study, we examined human embryos in which the NT was closing (Congenital Anomaly Research Center, Kyoto University) grossly and histologically, and found that NT closure in human embryos initiates at multiple sites but that the mode of NT closure in humans is different from that in many other animal species. In addition to the future cervical region that is widely accepted as an initiation site of NT closure (Site A), the mesencephalic-rhombencephalic boundary was found to be another initiation site (Site B). The second closure initiating at Site B proceeds bidirectionally and its caudal extension meets the first closure from Site A over the rhombencephalon, and the rostral extension of the second closure meets another closure extending from the rostral end of the neural groove (Site C) over the prosencephalon, where the anterior neuropore closes. The caudal extension of the first closure initiating at Site A was found to proceed all the way down to the caudal end of the neural groove where the posterior neuropore is formed, indicating that in humans, NT closure does not initiate at the caudal end of the neural groove to proceed rostrally. Since there is a considerable species difference in the mode of NT closure, we should be careful when extrapolating the data from other animals to the human. It seems that the type of NTD affects the intrauterine survival of abnormal embryos. Almost all the embryos with total dysraphism appear to die by 5 weeks of gestation, those with an opening over the rhombencephalon by 6.5 weeks, and those with a defect at the frontal and parietal regions survive beyond 7 weeks.
Anatomy and Embryology 07/2000; 201(6):455-66. · 1.42 Impact Factor
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ABSTRACT: To experimentally examine whether the pattern changes predicted by theoretical models of pattern formation actually occur in a limb bud cell culture system, we developed a practical method to automatically measure the periodicity of chondrogenic patterns in vitro. The method utilizes binary image processing to quantify the total number of peak and valley pixels in a pattern to obtain the average interval between stripes in the chondrogenic pattern, and we named it the peak length method. The reliability of the peak length method was examined by using computer simulation results. The peak length method enabled us quantitatively obtain the average interval between chondrogenic islands, and the values obtained by this method were closely correlated with the average intervals obtained by manual measurement and two-dimensional Fourier transformation. The average intervals obtained by the peak length method were shown to be stable over a wide range of pattern variations that are frequently observed in actual experiments. By applying the peak length method to actual experimental data, we compared the validity of two theoretical models of pattern formation (cell sorting model and reaction-diffusion model) and it was concluded that the peak-length method is a useful tool to quantitatively analyze chondrogenic patterns in limb micromass culture and to relate theoretical predictions and experimental results of pattern formation.
Anatomy and Embryology 06/2000; 201(5):419-28. · 1.42 Impact Factor
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H Kobayash,
R Doi,
R Hosotani,
Y Miyamoto,
T Koshiba,
K Fujimoto,
J Ida,
S Tsuji,
S Nakajima,
M Kawaguchi, K Shiota,
M Imamura
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ABSTRACT: The growth of both cancer cells and fetal tissue is rapid; however, cancer cells de-differentiate and proliferate in a disorderly manner, whereas fetal tissues differentiate and proliferate in an orderly manner. Thus, there may be both common and different factors that are involved in the process of the uncontrolled cell growth of pancreatic cancers and the development of the fetal pancreas. The common part of the mechanisms should be in the regulation of the cell cycle, resulting in rapid proliferation via such mechanisms as growth stimulation and avoidance of apoptosis. Therefore, in the current study we investigated the expression of apoptosis-related proteins in fetal pancreatic tissues.
Sixteen human embryonic and fetal pancreatic tissues obtained between 6 and 32 wk of gestation were used. We immunohistochemically examined the protein expression of Bcl-2, Bcl-XL, Mcl-1, and Bax. Further, the expression of insulin, glucagon, and proliferting cell nuclear antigen (PCNA), and TdT-mediated dUTP-biotin nick-end labeling (TUNEL) staining were examined.
In embryonic and fetal pancreatic tissues, Bcl-2 was not detected in any type of pancreatic cell (acinar, ductal, or islet). Bcl-XL was expressed in all types of pancreatic cells throughout the gestation. Mcl-1 was expressed in all types of pancreatic components, and strongly expressed in the margin of the islets. Bax, a pro-apoptotic protein, was expressed in all components. PCNA was strongly expressed in the embryonic and fetal pancreas, especially in early stages of gestation; however, TUNEL staining was negative in all samples. At least one antiapoptotic protein was expressed in all types of pancreatic cells.
The results of the current study indicate that active proliferation and avoidance of apoptosis take place in embryonic and fetal pancreatic tissues, which may be controlled by particular combinations of apoptosis-related proteins. Among these proteins, Bcl-XL and Mcl-1 may play an important role in the proliferation and differentiation of the embryonic and fetal pancreas.
International journal of pancreatology: official journal of the International Association of Pancreatology 05/2000; 27(2):113-22.
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ABSTRACT: It was previously speculated that TGFbeta acts as an "activator"-molecule in chondrogenic pattern formation in the limb micromass culture system, but its precise role and relationship with the cell sorting phenomenon have not been properly studied. In the present study, we examined whether the TGFbeta2 molecule satisfies the necessary conditions for an "activator"-molecule in the reaction-diffusion model. Firstly, we showed that TGFbeta2 became localized at chondrogenic sites during the establishment of a chondrogenic pattern, and exogenous TGFbeta2 promoted chondrogenesis when added in the culture medium. Secondly, TGFbeta2 protein was shown to promote the production of its own mRNA after 3 hr, indicating that a positive feedback mechanism exists which may be responsible for the emergence of the chondrogenic pattern. We then found that when locally applied with beads, TGFbeta2 suppressed chondrogenesis around the beads, indicating it induces the lateral inhibitory mechanism, which is a key element for the formation of the periodic pattern. We also examined the possible effects of TGFbeta2 on the cell sorting phenomenon and found that TGFbeta2 exerts differential chemotactic activity on proximal and distal mesenchyme cells of the limb bud, and at very early phases of differentiation TGFbeta2 promotes the expression of N-cadherin protein which is known to be involved in pattern formation in this culture system. These findings suggest that TGFbeta2 acts as an "activator"-like molecule in chondrogenic pattern formation in vitro, and is possibly responsible for the cell sorting phenomenon.
Developmental Dynamics 04/2000; 217(3):241-9. · 2.54 Impact Factor
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ABSTRACT: Various theoretical models have been proposed to explain the periodicity in the pattern of limb chondrogenesis, but experimental comparison of these models have seldom been performed properly. In the present study, micromass culture of limb bud mesenchyme cells was undertaken to test the validity of three theoretical models: the reaction-diffusion model, the cell sorting model, and the mechanochemical model. Computer simulations were undertaken to predict the factors that can affect the coarseness of the chondrogenic pattern. According to the predictions, we performed micromass culture of limb mesenchyme in collagen and agarose gel. Then we carried out time-lapse observation to analyze the cell movement during pattern formation. From computer simulations it was theoretically predicted that changes in the surrounding extracellular matrix should alter the periodicity of the chondrogenic pattern in vitro, and we found that pattern changes actually occurred under different culture conditions. When compared with the culture in a liquid medium, the chondrogenic pattern became less coarse when the cells were cultured in collagen or agarose gel, and the pattern change appeared to be independent of the cell differentiation. Time-lapse observation revealed a decrease in cell motility when the cells were cultured in gel. It was found that both the reaction-diffusion and cell sorting models fit the pattern change produced and that the mechanochemical model is not primarily important in the chondrogenic pattern formation in vitro.
The Anatomical Record 02/2000; 258(1):100-7.
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ABSTRACT: Although oxygen is essential for promoting energy metabolism and for enhancing cell proliferation, early mouse embryos are very sensitive to high oxygen concentration. Because the tissue-specificity and sequential changes of the expression of antioxidative enzymes in rodent embryos have not been investigated systematically, we examined the ontogenesis of thioredoxin (TRX) and glutaredoxin (GRX) in mouse embryos and fetuses by using immunohistochemical methods. These compounds were found to be localized in most tissues examined, with some tissue specificity and temporal sequence. In many tissues, both TRX and GRX began to be expressed at embryonic day 11 (E11) or E13 and appeared to increase later in development, but the heart and great vessels of E8.5 embryos were already positive for their immunoreactivity. The stage at which the antioxidative enzymes begin to be expressed seems to coincide with the stage at which rodent embryos acquire the capacity of aerobic energy metabolism. Although TRX and GRX were co-localized in many tissues and showed similar sequential changes of expression, their expression patterns were different in the fetal cartilage, suggesting that they may play different roles in endochondral ossification. Their immunoreactivity was not homogeneous in the liver and the epithelium of uriniferous tubules, probably because their expression is associated with the proliferating and metabolic activities of the cell, as suggested by previous investigators. These results suggest that TRX and GRX play some tissue-specific roles in mammalian morphogenesis as well as general roles as antioxidant enzymes.
Antioxidants and Redox Signaling 02/2000; 2(4):653-63. · 8.46 Impact Factor
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ABSTRACT: To investigate the heat shock effects upon somitogenesis and specification of the vertebral identity, pregnant ICR mice were briefly exposed to 42 degrees C or 43 degrees C at E7.5, E8.5, or E9.5 (noon of the plug day = E0.5). Heat treatment induced embryonic day-specific vertebral transformations whose frequency and severity were dependent on the temperature elevation. Following a heat treatment at E8.5, the vertebral identity of T6 through S1 was shifted anteriorly by one or two segments (posterior transformations). Such shifts were found in more than one-third of the fetuses heat-stressed at 42 degrees C, and in over 90% of those exposed to 43 degrees C. When heated at E7.5, the anterior boundary of vertebral transformations was shifted cranially to cervical levels (C1-C7), and when heated at E9.5, it was shifted caudally to the lower thoracic and lumbar levels (T13-L4). Examination of Hox gene expression domains by in situ hybridization showed that the anterior boundaries of Hoxa-5, Hoxa-7, Hoxc-8, and Hoxc-9 expression domains in the paraxial mesoderm were shifted cranially by one somite segment in embryos heated at E7.5, as compared with the corresponding levels of their expression in control embryos. Such cranial shifts were found for Hoxa-7, Hoxc-8 and Hoxc-9, but not for Hoxa-5, in embryos heated at E8.0. In embryos heated at E8.5, only the expression domains for Hoxc-8 and Hoxc-9 were found to be shifted. The observed stage-specific vertebral transformations and shifts of the Hox gene expression domains were consistent with the temporal colinearity and posterior predominance of Hox gene expression during development. Further histological and cytochemical analyses revealed that heat-induced vertebral transformations may not be a result of induced cell death, but heat-induced transient arrest of cell proliferation and somitogenesis could result in altered expression of Hox genes and subsequently produce vertebral transformations.
Developmental Dynamics 01/2000; 216(4-5):336-48. · 2.54 Impact Factor
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ABSTRACT: Neural tube defects (NTD) are a group of malformations that result from the failure of the neural tube to close early in embryonic development and among the most common congenital malformations in humans. It has been reported that a substantial proportion of NTD in humans can be prevented by folic acid (FA) supplementation prior to conception and during the first months of pregnancy, and myo-inositol (MI) was shown to reduce the incidence of NTD in curly tail mice which are not prevented by FA. Brief maternal hyperthermia (HT) early in pregnancy has been implicated in NTD both in humans and laboratory animals, and anterior NTD including exencephaly and anencephaly are induced frequently when pregnant mice are exposed to HT. We examined the effect of FA or MI supplementation of pregnant mice on the occurrence of heat-induced NTD in the offspring. When pregnant mice were treated with FA (3 mg/kg) daily from gestational day (GD) 0.5 through GD 9.5 and heated at GD 8.5, the prevalence of NTD in the fetuses (26.6%) was significantly lower than the corresponding figure in the HT alone group (38.6%; P < 0.05). However we failed to detect the preventive effect of MI (500 mg/kg). The results of this study suggest that prenatal FA supplementation decreases HT-induced NTD in mice and sufficient FA intake during early pregnancy may be recommended to avoid the birth of malformed children.
Journal of Nutrition 11/1999; 129(11):2070-3. · 3.92 Impact Factor
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Nō to shinkei = Brain and nerve 09/1999; 51(8):659-66.
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ABSTRACT: The present study investigated the occurrence of apoptotic cell death in the mouse testis at various intervals following the administration of hydroxyurea (HU). The presence of apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) method and by DNA fragmentation assay using ligation-mediated polymerase chain reaction. Both the incidence of apoptotic cells and the level of DNA fragmentation in the testis increased depending on the HU dose, and they were most apparent at the highest dose (400 mg/kg). The incidence of apoptotic cells in the HU-treated group increased continuously and peaked at 12 h, but then decreased gradually, reaching control levels by 48 h. After HU treatment, TUNEL-positive apoptotic cells increased in the seminiferous epithelium of the tubules, and affected cells were found synchronously in the tubules of animals treated with HU. Spermatogonia and spermatocytes were found to be affected selectively. TUNEL-positive cells were found to be stage-specific and were primarily in stage IV-VI tubules. It has been shown that in vivo HU exposure induced testicular germ cell apoptosis dose dependently in a time- and stage-specific manner, and damaged cells appeared to be eliminated by phagocytosis by neighboring cells. Apoptosis of damaged testicular germ cells is apparently a common response to various testicular toxicants therefore protecting the next generations of germ cells from the damaged cell population.
Toxicology and Applied Pharmacology 04/1999; 155(2):139-49. · 4.45 Impact Factor
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ABSTRACT: Attempts to gain a better understanding of the relationship between the epidermal ridge patterns (dermatoglyphics) and flexion creases on the volar aspects of human hands and feet and specific medical disorders led to a search for a suitable animal model, allowing studies of the fetal development of the pertinent structures. A common experimental animal, the rat (Rattus norvegicus), was found to be an excellent candidate, owing to the strong resemblance of the volar pads and flexion creases on its palmar and plantar surfaces to those of human subjects. A hereditary preaxial polydactyly mouse (Pdn) provides an opportunity to study the effects of this malformation on the surrounding morphological structures and, specifically, on the volar pads, i.e., the sites over which the dermatoglyphic patterns develop. The hands and feet of the wild-type (+/+) mice show no anomalies, and their major pad and flexion crease configurations correspond to those of normal rats. The heterozygous (Pdn/+) mice, in spite of having a thumb/big toe with a duplicated distal phalanx on their hands/feet, did not display any alterations in palmar/plantar pads. The homozygous (Pdn/Pdn) mice have a protrusion in the thenar area and one to three supernumerary digits on the preaxial portion of both the hands and feet. The effect of these anomalies was found to be limited to the pad and flexion crease configurations in the preaxial areas; the postaxial sites were not affected. The original number of pads on the thenar/first interdigital areas of Pdn/Pdn mice was apparently identical to that of the +/+ and Pdn/+mice. The preaxial protrusion, however, affected the number, size, and location of the pads observed in the newborn mice, resulting in varying pad configurations, such as fused and scattered pads or a pad cluster formed by gathering the neighboring pads. These pad modifications were induced by the preaxial plantar/palmar protrusion only and were not affected by the presence of supernumerary preaxial digits. In view of the similarities in the morphology and fetal development of human and mouse distal limbs, the present study is relevant to human subjects, particularly to the understanding of the significance of dermatoglyphic variations in individuals with specific medical disorders. Future studies of naturally occurring or experimentally induced limb malformations in mice or rats should provide valuable insights into the development of human hands and feet and into factors contributing to their congenital anomalies.
Journal of Morphology 02/1999; 239(1):87-96. · 1.54 Impact Factor
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ABSTRACT: Expression of 105 k-Da heat shock protein (HSP105) during mouse embryo development was investigated. Although HSP105 was detected scarcely in mouse embryos at gestational day (GD) 8, its level of HSP105 increased markedly in the embryos from GD 9 to 11, and then decreased gradually by GD 14. In contrast, 70 k-Da heat shock cognate protein (HSC70) was detected at constantly high levels in embryo from GD 8 to 17 (before birth). The transient increase in level of HSP105 was observed in most embryonic tissues. Since the levels of HSP105 mRNA was detected at constantly high levels in the embryos between GD 8 and 12, the increased expression of HSP105 at GD 9 to 11 seemed to be regulated at posttranscriptional level. Immunohistochemically, HSP105 as well as HSC70 were localized in the cytoplasm and the nuclei of cells in various mouse embryonic tissues. After treatment of tissue sections with proteinase K, HSP105 but not HSC70 was also found to be localized in condensed cells and condensed bodies which showed the typical characteristics of apoptotic cells and apoptotic bodies at the interdigital regions of limbs. These findings suggest that HSP105 plays important roles during mouse embryo development.
Cell Structure and Function 11/1997; 22(5):517-25. · 2.29 Impact Factor
