Journal of physiology and biochemistry (J PHYSIOL BIOCHEM)

Publisher: Springer Verlag

Current impact factor: 1.97

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 1.969
2013 Impact Factor 2.496
2012 Impact Factor 1.654
2011 Impact Factor 1.711
2010 Impact Factor 1.357
2009 Impact Factor 0.891
2008 Impact Factor 1.172
2007 Impact Factor 1.264
2006 Impact Factor 1.362
2005 Impact Factor 0.934
2004 Impact Factor 0.758
2003 Impact Factor 0.564
2002 Impact Factor 0.696
2001 Impact Factor 0.639
2000 Impact Factor 0.958
1999 Impact Factor 0.385
1998 Impact Factor 0.491
1997 Impact Factor 0.067

Impact factor over time

Impact factor

Additional details

5-year impact 2.04
Cited half-life 3.70
Immediacy index 0.31
Eigenfactor 0.00
Article influence 0.49
Website Journal of Physiology & Biochemistry website
Other titles Journal of physiology and biochemistry (Online)
ISSN 1138-7548
OCLC 70708332
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

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    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
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    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification

Publications in this journal

  • Ming-ming Ni · Tao Xu · Ya-rui Wang · Ying-hua He · Qun Zhou · Cheng Huang · Xiao-ming Meng · Jun Li ·

    Journal of physiology and biochemistry 11/2015; DOI:10.1007/s13105-015-0452-6
  • Carol Moreno · María T. Llinás · Francisca Rodriguez · Juan M. Moreno · F. Javier Salazar ·

    Journal of physiology and biochemistry 11/2015; DOI:10.1007/s13105-015-0450-8
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    ABSTRACT: Myeloid leukemia factor 1 (MLF1) was involved in t(3;5) chromosomal rearrangement and aberrantly expressed in myelodysplastic syndromes/acute myeloid leukemia patients. Ex vivo experiments showed that the lymphocytes from the Mlf1-deficient mice were more resistant to apoptotic stimulations than the wild-type cells. Furthermore, the ectopically expressed MLF1 induced apoptosis in the cell models. These findings revealed that MLF1 was required for the cells to respond to the apoptotic stimulations. Ex vivo experiments also demonstrated that cytokine withdrawal significantly up-regulated Mlf1's expression and promoted its association with B cell lymphoma-extra large (Bcl-XL) in the lymphocytes, at the same time reduced the association of Bax with Bcl-XL The same effects were also observed in the cells that over-expressed MLF1. However, these effects were observed in Mlf1 null lymphocytes as well as the cells over-expressing Bcl-XL. In addition, MLF1's proapoptosis could be completely prevented by co-expression of Bcl-XL and significantly attenuated in Bax/Bak double null cells. These data, taken together, strongly suggested that in response to the stresses, up-regulated Mlf1 promoted its association with Bcl-XL and reduced the available Bcl-XL for associating with Bax, which resulted in releasing Bax from the Bcl-XL and apoptosis in turn. Lastly, we showed that MLF1 was negatively regulated by 14-3-3 and revealed that 14-3-3 bound to MLF1 and physically blocked MLF1's Bcl-2 homology domain 3 (BH3) as well as Bcl-XL from associating with MLF1. Our findings suggested that ectopically expressed MLF1 could be responsible for the pathological apoptosis in early myelodysplastic syndrome (MDS) patients.
    Journal of physiology and biochemistry 11/2015; DOI:10.1007/s13105-015-0445-5
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    ABSTRACT: To investigate whether uric acid could regulate urate transporter 1 (URAT1) protein and activity level, we established uric acid nephropathy (UAN) rat model and detected their serum uric acid and URAT1 level with or without the treatment of allopurinol. Results here showed that allopurinol could reduce serum uric acid level in UAN rat model. We further found that in UAN rats, the total and surface URAT1 expression level were both increased while this increase could be blocked by allopurinol treatment. By treating URAT1 stable expressed HEK cell with monosodium urate (MSU) crystals, we found that URAT1 level showed an increase in both total and cell surface level, and it would colocalize more with Rab11 instead of Rab7. Consistently, we also found that the total URAT1 protein level will show an increase in the presence of lysosome inhibitors but not ubiquitin-proteasome inhibitors. Furthermore, we also found that MSU crystal could drive Numb, a clathrin-coated adaptor protein which performs a key function in cell division, out of cell surface and disassociated it from URAT1. Finally, we found that Numb short hairpin RNA (shRNA)-transfected showed a phenocopy as MSU treatment, while Numb-2A mutation over-expression could resist crystal-induced phenotypes. These findings indicated that uric acid crystal could increase URAT1 membrane distribution through inhibiting Numb-induced URAT1 lysosome degradation.
    Journal of physiology and biochemistry 03/2015; 71(2). DOI:10.1007/s13105-015-0399-7
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    ABSTRACT: Previous studies have demonstrated inconsistent roles of Rho kinase (ROCK) in the decreased vasoconstriction of rat hindquarter vessels induced by hindlimb unweighting (HU). The present study was designed to determine the unclear role of ROCK in the mediation of HU-induced decreased femoral arterial vasoconstriction. 28-day HU rat was adopted as the animal model. With or without Y-27632, a ROCK inhibitor, isometric force of femoral artery was measured. The expression of ROCK and its effects on downstream targets were also examined. Results showed that (1) HU caused a significant decrease of the phenylephrine (PE)-evoked and potassium chloride (KCl)-evoked femoral arterial vasoconstriction (P < 0.05), confirming the functional findings by previous studies. (2) Inhibition of ROCK with Y-27632 produced an equal reduction of the vasoconstriction in CON and HU. (3) HU significantly decreased ROCK II expression and the effects of ROCK on myosin light-chain phosphatase (MLCP) and MLC (P < 0.05), but increased p65 nuclear translocation (P < 0.05) and inducible nitric oxide synthase (iNOS) expression (P < 0.05). (4) HU significantly (P < 0.05) increased NO production in femoral arteries, with Y-27632 significantly (P < 0.01) amplifying this effect. These findings have revealed that 28-day HU reduced the expression and effects of ROCK on downstream targets both directly (MLCP and MLC) and possibly indirectly (NF-κB/iNOS/NO pathway) related to vasoconstriction in femoral arteries.
    Journal of physiology and biochemistry 03/2015; 71(2). DOI:10.1007/s13105-015-0398-8
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    ABSTRACT: Experimental and clinical evidences suggest that apelin and its receptor APJ are involved in the pathogenesis of cardiovascular complications. However, the role of apelin/APJ in hypertension is not sufficiently understood. Because chronic kidney diseases lead to hypertension and cardiac failure, we investigated the changes in apelin receptor gene expression in the myocardium and aorta of rat models of kidney disease hypertension. Two-kidney, one-clip (2K1C) hypertension was produced by placing a clip around the renal artery. Four and 16 weeks later, blood pressure, left ventricular end-diastolic pressure (LVEDP), serum apelin, and angiotensin II were measured. The messenger RNA (mRNA) and protein of APJ were determined by reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. Chronic hypertensive rats had approximately 10 times higher LVEDP (P < 0.001). 2K1C decreased serum apelin from 220 ± 11 to 170 ± 10 pg/mL in 16 weeks (P < 0.05). The mRNA expression of APJ significantly decreased in the heart and aorta at 4 weeks. At 16 weeks, the reduction was not significant in the heart but was significant in the aorta. At 4 weeks, the expression of the APJ protein significantly decreased in the heart but not in the aorta. At 16 weeks, APJ protein was significantly decreased only in the aorta. Reduction of serum apelin and downregulation of apelin receptors in both the heart and aorta may play a role in the pathophysiology of hypertension and cardiac failure in 2K1C hypertensive rats.
    Journal of physiology and biochemistry 02/2015; 71(2). DOI:10.1007/s13105-015-0394-z
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    ABSTRACT: Orosomucoid (ORM), or alpha-1-acid glycoprotein (AGP), is one of the acute-phase proteins. It has a molecular weight of 37-54 kDa, low pI of 2.8-3.8, and is heavily glycosylated (45 %). It is mainly synthesized by the liver, but many extrahepatic tissues have also been reported to produce ORM under myriad physiological and pathological conditions. Expression of the ORM gene is mainly controlled by a combination of the major regulatory mediators, such as glucocorticoids, interleukin (IL)-1, TNF-α, and IL-6. ORM has many activities including, but not limited to, acting as an acute-phase reactant and disease marker, modulating immunity, binding and carrying drugs, maintaining the barrier function of capillary, and mediating the sphingolipid metabolism. Its related receptor has been preliminarily explored in macrophages, neutrophils, and liver parenchymal cells, involving the membrane receptor CCR5, Siglect-5, and HBB, respectively. Additional activities of ORM such as regulating metabolism are currently being explored. Because of its regulation in liver diseases, cancer, and HIV, future ORM research is warranted.
    Journal of physiology and biochemistry 02/2015; 71(2). DOI:10.1007/s13105-015-0389-9
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    ABSTRACT: Obesity is defined as an excessive accumulation of adipose tissue that may lead to health complications. Mounting evidence indicates that obesity has a negative impact on fertility. Yet, the link between adipose tissue biology and infertility remains unclear. We aimed to investigate the communication between the adipose tissue and the reproductive system and the importance of this cross talk for the development of a receptive endometrium. To that end, we generated an in vitro model with endometrial and adipocyte cell lines. Sexual hormones, progesterone and estradiol, were used to decidualize endometrial cells and sensitize adipocytes. Decidualization produced a simultaneous increase of adipokine receptors in endometrial cells paralleling changes in their receptivity status. Furthermore, sensitization of 3T3-L1 adipocytes increased mRNA levels of leptin and resistin and decreased the expression of adiponectin and chemerin levels. This was accompanied by increased isoproterenol-induced lipolysis and reduced insulin-stimulated glucose uptake. Lastly, conditioned culture medium of those sensitized adipocytes was used to feed endometrial cells. This treatment resulted in (i) upregulation of genes previously identified as positive regulators of endometrial receptivity, such as leukemia inhibitory factor and glutathione peroxidase 3, and (ii) downregulation of interleukin-15 and mucin1, both genes negatively related with endometrial receptivity. Our results indicate that the endocrine communication between adipose tissue and the reproductive system is bidirectional and stress the importance of the adipose tissue to modulate the reproductive fitness.
    Journal of physiology and biochemistry 02/2015; 71(3). DOI:10.1007/s13105-015-0393-0
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    ABSTRACT: The mechanisms underlying the relationships between nutritional status and immunity remain to be fully characterized. The present study was undertaken to analyze by flow cytometry, in the context of diet-induced obesity, the status of immune cells in subcutaneous, and epididymal fat depots in wild-type and immunodeficient Rag2-/- mice submitted to nutritional challenge, i.e., 48-h fasting and 1-week refeeding. In parallel, the responsiveness of mature adipocytes and immune cells in bone marrow, lymph node, and liver were also analyzed. The results show that fasting in obese wild-type mice induces a prominent lipolysis in epididymal AT and immunosuppression restricted to both subcutaneous and epididymal AT, characterized by reduced number of CD4+ T and B lymphocytes and M1/M2 macrophages associated with reduced leptin and increased FGF21 expression in mature adipocytes. One-week refeeding was sufficient to reverse the fasting-induced effects. Obese immunodeficient mice under nutritional challenge exhibited no changes in adipocyte leptin expression and no marked trafficking of AT macrophages or NK cells, while the fasted-induced upregulation of FGF21 expression was maintained as well as the lipolytic responses. The present results demonstrate that, in a context of diet-induced obesity, fasting-induced immunosuppression is restricted to fat depots in immunocompetent mice. Lack of adipocyte leptin regulation and fasting-induced immunosuppression in obese immunodeficient mice strongly suggests that lymphocytes are involved in the modulation of adipocyte leptin expression on one hand and on the other that leptin is involved in the immune changes in AT according to nutritional status.
    Journal of physiology and biochemistry 02/2015; 71(3). DOI:10.1007/s13105-015-0388-x
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    ABSTRACT: Carbon monoxide (CO) is critical in cell signaling, and inhalation of gaseous CO can impact cardiovascular physiology. We have investigated electrophysiological effects of CO and their potential cGMP-dependent mechanism in isolated preparations of murine myocardium. The standard microelectrode technique was used to record myocardial action potentials (APs). Exogenous CO (0.96 × 10−4–4.8 × 10−4 M) decreased AP duration in atrial and ventricular tissue and accelerated pacemaking activity in sinoatrial node. Inhibitors of heme oxygenases (zinc and tin protoporphyrin IX), which are responsible for endogenous CO production, induced the opposite effects. Inhibitor of soluble guanylate cyclase (sGC), ODQ (10−5 M) halved CO-induced AP shortening, while sGC activator azosidnone (10−5 M-3 × 10−4 M) and cGMP analog BrcGMP (3 × 10−4 M) induced the same effects as CO. To see if CO effects are attributed to differential regulation of phosphodiesterase 2 (PDE2) and 3 (PDE3), we used inhibitors of these enzymes. Milrinone (2 × 10−6 M), selective inhibitor of cGMP-downregulated PDE3, blocked CO-induced rhythm acceleration. EHNA(2 × 10−6 M), which inhibits cGMP-upregulated PDE2, attenuated CO-induced AP shortening, but failed to induce any positive chronotropic effect. Our findings indicate that PDE2 activity prevails in working myocardium, while PDE3 is more active in sinoatrial node. The results suggest that cardiac effects of CO are at least partly attributed to activation of sGC and subsequent elevation of cGMP intracellular content. In sinoatrial node, this leads to PDE3 inhibition, increased cAMP content, and positive chronotropy, while it also causes PDE2 stimulation in working myocardium, thereby enhancing cAMP degradation and producing AP shortening. Thus, CO induces significant alterations of cardiac electrical activity via cGMP-dependent mechanism and should be considered as a novel regulator of cardiac electrophysiology.
    Journal of physiology and biochemistry 02/2015; DOI:10.1007/s13105-015-0387-y
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    ABSTRACT: Type 2 diabetes (T2D) is a complicated systemic disease, and the exact pathogenetic molecular mechanism is unclear. Distinct histone modifications regulate gene expression in certain diseases, but little is known about histone epigenetics in diabetes. In the current study, C57BL/6 J mice were used to build T2D model, then treated with exendin-4 (10 μg/kg). Histone H3K9 and H3K23 acetylation, H3K4 monomethylation and H3K9 dimethylation were explored by Western blotting of liver histone extracts. Real-time polymerase chain reaction (PCR) was used to examine expression levels of diabetes-related genes, while chromatin immunoprecipitation (ChIP) was applied to analyze H3 and H3K9 acetylation, H3K4 monomethylation, and H3K9 dimethylation in the promoter of facilitated glucose transporter member 2 (Glut2) gene. The results showed that liver's total H3K4 monomethylation and H3K9 dimethylation was increased in diabetic mice, which was abrogated with the treatment of exendin-4. In contrast, H3K9 and H3K23 acetylation were reduced in diabetic mice, while exendin-4 only alleviated the reduction of H3K9 acetylation. Our data indicated that the progression of type 2 diabetes mellitus (T2D) is associated with global liver histone H3K9 and H3K23 acetylation, H3K4 monomethylation, and H3K9 dimethylation. Exploiting exact histone modify enzyme inhibitors, which may represent a novel strategy to prevent T2D.
    Journal of physiology and biochemistry 02/2015; 71(1). DOI:10.1007/s13105-015-0385-0
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    ABSTRACT: Myosin light chain kinase (MLCK) may play a key role in cellular contraction, paracellular permeability and lung water homeostasis. In vitro, thyroid hormones (THs) potently inhibit MLCK activation and, hence, MLC phosphorylation. Whether similar effect is exerted by THs in in vivo systems is not known. Therefore, we investigated the effects of hypothyroid (HO) and hyperthyroid (HR) states on the level of phospho-MLC, aquaporin 5 (AQP5) protein expression, and water holding capacity in the rat lung. Alterations in thyroid state were induced by adding methimazole or levothyroxine (L-T4) to animals’ drinking water. Serum TH concentration and thyroid gland histomorphology were assessed to verify the onset of the thyroid state. Lung phospho-MLC and AQP5 proteins were assessed by Western blotting and immunohistochemistry. Lung extravascular water content was estimated by the tissue wet weight-to-dry weight (W/D) ratio. The HO state induced significant increases in the expression of lung phospho-MLC and AQP5 proteins. In contrast, the HR state caused moderate decreases in lung phospho-MLC and AQP5 proteins. While lung water holding capacity was significantly increased in HO animals, it was significantly reduced in HR animals. The data of this study show that THs are able to modulate MLC phosphorylation in in vivo systems. Besides, they suggest that the circulating level of THs may alter lung fluid balance not only through expression of water channels but also through regulation of cellular contraction and paracellular permeability.
    Journal of physiology and biochemistry 02/2015; 71(1). DOI:10.1007/s13105-015-0386-z