Maohong Cao

Nantong University, Tungchow, Jiangsu Sheng, China

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Publications (21)53.95 Total impact

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    ABSTRACT: Hyperphosphorylation and dysregulation of exon 10 splicing of tau are pivotally involved in pathogenesis of Alzheimer's disease (AD) and/or other tauopathies. Alternative splicing of tau exon 10, which encodes the second microtubule-binding repeat, generates tau isoforms containing three and four microtubule-binding repeats, termed 3R-taus and 4R-taus, respectively. Dual-specificity tyrosine-phosphorylation-regulated kinase 1A (Dyrk1A) lies at the Down syndrome critical region of chromosome 21. Overexpression of this kinase may contribute to the early tau pathology in Down syndrome via phosphorylation of tau and dysregulation of tau exon 10. Here, we report that Dyrk1A was truncated at C-terminus and was associated with over-activation of calpain I in AD brain. Calpain I proteolyzed Dyrk1A in vitro first at the C-terminus and further at the N-terminus and enhanced its kinase activity towards tau via increased Vmax, but not Km. C-terminal truncation of Dyrk1A resulted in stronger activity than its full-length protein in promotion of exon 10 exclusion and phosphorylation of tau. Dyrk1A was truncated in kainic acid-induced-excitotoxic mouse brains and coincided with an increase in 3R-tau expression and phosphorylation of tau via calpain activation. Moreover, truncation of Dyrk1A was correlated with an increase in the ratio of 3R-tau/4R-tau and tau hyperphosphorylation in AD brain. Collectively, these findings suggest that truncation/activation of Dyrk1A by Ca2+/calpain I might contribute to tau pathology via promotion of exon 10 exclusion and hyperphosphorylation of tau in AD brain. Copyright © 2015, The American Society for Biochemistry and Molecular Biology.
    Journal of Biological Chemistry 04/2015; 290(24). DOI:10.1074/jbc.M115.645507 · 4.57 Impact Factor
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    ABSTRACT: Abnormal hyperphosphorylation of tau is pivotally involved in the pathogenesis of Alzheimer's disease (AD) and related tauopathies. Glycogen synthase kinase 3β (GSK-3β) is a primary tau kinase that is most implicated in tau pathology in AD. However, the exact molecular nature of GSK-3β involved in AD is unclear. In the present study, we found that GSK-3β was truncated at C-terminus and correlated with over-activation of calpain I in AD brain. Truncation of GSK-3β was positively correlated with tau hyperphosphorylation, tangles score and Braak stage in human brain. Calpain I proteolyzed GSK-3β in vitro at C-terminus, leading to an increase of its kinase activity, but keeping its characteristic to preferentially phosphorylate the protein kinase A-primed tau. Excitotoxicity induced by kainic acid (KA) caused GSK-3β truncation at C-terminus and hyperphosphorylation of tau in mouse brain. Inhibition of calpain prevented the KA-induced changes. These findings suggest that truncation of GSK-3β by Ca(2+)/calpain I markedly increases its activity and involvement of this mechanism probably is responsible for up-regulation of GSK-3β and consequent abnormal hyperphosphorylation of tau and neurofibrillary degeneration in AD.
    Scientific Reports 02/2015; 5:8187. DOI:10.1038/srep08187 · 5.58 Impact Factor
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    ABSTRACT: Cyclin-dependent kinase-5 (CDK5), a serine/threonine kinase which can be activated by its neuron-specific activator p35, or its truncated form p25, plays an important role in a variety of neuronal events, including neuronal migration, synaptic transmission, and neuronal death. Accumulating evidence has shown that abnormal activation of CDK5 was a critical neuronal pro-death signal in central nervous system (CNS) diseases. However, it remains unclear how CDK5 functions upon neuronal apoptosis following intracerebral hemorrhage (ICH). In the present study, we established ICH models by injecting autologous whole blood into the right basal ganglia of adult rats and assessed their neurological deficits by behavioral tests. CDK5 protein levels and kinase activities were upregulated adjacent to the hematoma following ICH. Immunofluorescent staining showed CDK5 was mainly localized in neurons, rather than in astrocytes or oligodendrocytes. Furthermore, active caspase-3, an apoptotic marker, showed a temporally parallel expression with the protein levels/kinase activities of CDK5 following ICH. Meantime, myocyte enhancer factor 2D (MEF2D), a pro-survival transcription factor which could be phosphorylated inactivation by CDK5, also exhibited high phosphorylation levels following ICH. In vitro, we obtained a consistent upregulation of CDK5 kinase activity in primary cortical neurons after thrombin treatment. Knocking down CDK5 kinase activity suppressed neuronal apoptosis and coupled with reduced MEF2D phosphorylation at ser(444) residues. Thus, we speculated that CDK5 might exert an important function in the regulation of neuronal apoptosis following ICH.
    Journal of Molecular Neuroscience 11/2014; 56(1). DOI:10.1007/s12031-014-0466-5 · 2.76 Impact Factor
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    ABSTRACT: The novel Krüppel-like zinc finger protein Gli-similar 2 (Glis2), one member of the transcription factors, is involved in controlling the flow of genetic information and the modulation of diverse cellular activities. Accumulating evidence has demonstrated its important roles in adult development and several diseases. However, information regarding the regulation and possible function of Glis2 in the central nervous system is still limited. In this study, we explored the roles of Glis2 during the pathophysiological process of intracerebral hemorrhage (ICH). An ICH rat model was established and assessed by behavioral tests. Expression of Glis2 was significantly up-regulated in brain areas surrounding the hematoma following ICH. Immunofluorescence showed that Glis2 was strikingly increased in neurons, but not astrocytes or microglia. Up-regulation of Glis2 was found to be accompanied by the increased expression of active caspase-3 and Bax and decreased expression of Bcl-2 in vivo and vitro studies. Moreover, knocking down Glis2 by RNA-interference in PC12 cells reduced active caspase-3 and Bax expression while increased Bcl-2. Collectively, we speculated that Glis2 might exert pro-apoptotic function in neurons following ICH.
    Cellular and Molecular Neurobiology 11/2014; 35(3). DOI:10.1007/s10571-014-0130-1 · 2.20 Impact Factor
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    ABSTRACT: To study whether Lrp11 is involved in stress response and find its expression regulatory network, the model of stress has been built using C57BL/6J (B6) and DBA/2 (D2) mice. Western blotting, qPCR and immunohistochemistry were used to investigate the expression variation of Lrp11 in amygdala tissue after exposure to stress. We found the quantity of Lrp11 was more obvious in stress models than that in normal mice (P<0.05) which suggests Lrp11 might participate in the process of stress response. The expression of Lrp11 is controlled by a cis-acting quantitative trait locus (cis-eQTL). We identified four genes that are regulated by Lrp11 and the expression of 66 genes highly correlated with Lrp11, seven of which have previously been implicated in stress pathways. To evaluate the relationship between Lrp11 and its downstream genes or network members, we transfected HEK 293T cells and SH-SY5Y cells with Lrp11 siRNA leading to down-regulation of Lrp11mRNA and were able to confirm a significant influence of Lrp11 depletion on the expression of Xpnpep1, Maneal, Pgap1 and Uprt. These validated downstream targets and members of Lrp11 gene network provide new insight into the biological role of Lrp11 and may be an important risk factor in the development of stress.
    Psychiatry Research 09/2014; 220(3). DOI:10.1016/j.psychres.2014.09.002 · 2.68 Impact Factor
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    ABSTRACT: Podoplanin (PDPN) is a mucin-type transmembrane sialoglycoprotein expressed in multiple tissues in adult animals, including the brain, lungs, kidney, and lymphoid organs. Studies of this molecule have demonstrated its great importance in tumor metastasis, platelet aggregation, and lymphatic vessel formation. However, information regarding its regulation and possible function in the central nervous system is still limited. In this study, we performed a neuroinflammatory model by lipopolysaccharide (LPS) lateral ventral injection in adult rats and detected increased expression of PDPN in the brain cortex. Immunofluorescence indicated that PDPN was located in the neurons, but not astrocytes. Moreover, there was a concomitant up-regulation of active caspase-3, cyclin D1, and CDK4 in vivo and vitro studies. In addition, the expression of these three proteins in cortical primary neurons was decreased after knocking down PDPN by siRNA. Collectively, all these results suggested that the up-regulation of PDPN might be involved in neuronal apoptosis in neuroinflammation after LPS injection.
    Cellular and Molecular Neurobiology 05/2014; 34(6). DOI:10.1007/s10571-014-0060-y · 2.20 Impact Factor
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    ABSTRACT: EHD2, a member of the Eps15 homology domain (EH domain) family, is important for protein interactions during vesicular trafficking. Previous studies have proved that EHD2 can regulate trafficking from the plasma membrane in the process of endocytosis. However, its function in central nervous system diseases is still with limited understanding. In this frame, we found that EHD2 expression was upregulated in the perihematomal caudate in adult rats after intracerebral hemorrhage (ICH). Double immunofluorescence staining revealed that EHD2 was colocalized with neurons and activated microglias after ICH. Besides, we detected that neuronal apoptosis markers (TUNEL and caspase-3), and microglial activation marker (CD68), also known as a marker of macrophage, were colocated with EHD2. The vitro study also indicated that EHD2 was linked with neuronal apoptosis and microglial phagocytosis. All our findings suggested that EHD2 might be involved in the pathophysiology of ICH.
    Journal of Molecular Neuroscience 03/2014; DOI:10.1007/s12031-014-0271-1 · 2.76 Impact Factor
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    ABSTRACT: SYF2, known as CCNDBP1-interactor or p29, is likely involved in pre-mRNA splicing and cell cycle progression. The present study was designed to elucidate dynamic changes in SYF2 expression and distribution in the cerebral cortex in a lipopolysaccharide (LPS)-induced neuroinflammation rat model. It was found that SYF2 expression was induced strongly in active astrocytes after LPS injection. In vitro studies showed that the upregulation of SYF2 might be involved in the activation of C6 cells after LPS challenge and the neuronal apoptosis after conditioned media challenge. In addition, with silencing of SYF2 in C6 and PC12 cells by siRNA, the results indicated that SYF2 was required for astrocyte activation and neuronal apoptosis induced by LPS. Our findings on the cellular signaling pathway may provide a new therapeutic strategy against neuroinflammation in the CNS. © 2013 Wiley Periodicals, Inc.
    Journal of Neuroscience Research 03/2014; 92(3). DOI:10.1002/jnr.23312 · 2.73 Impact Factor
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    ABSTRACT: Wild type p53-induced phosphatase 1 (Wip1) is a phosphatase which belongs to protein phosphatase type 2C family, which have been predominantly linked to cell growth and to cellular stress signaling. Numerous downstream targets of Wip1 have been identified, and genetic studies confirm that some play a part in tumorigenesis. Recent evidence highlights a new role for Wip1 in the regulation of NF-κB p65, which indicated that it might play a critical role in immune system. However, its regulation role in central nervous system (CNS) remains poorly understood. To elaborate whether Wip1 was involved in CNS injury, we performed a neuroinflammatory model by lipopolysaccharide (LPS) lateral-ventral injection in adult rats. Wip1 expression was strongly upregulated in active astrocytes in inflamed brain cortex. In vitro studies indicated that the upregulation of Wip1 may be involved in the subsequent astrocytic activation following LPS exposure, and knockdown of Wip1 in primary astrocytes by siRNA showed that Wip1 inhibited the synthesis of TNF-α. Collectively, these results suggested that Wip1 may be important in host defense in CNS immune response, which might provide a potent therapeutic target of neuroinflammation.
    Journal of Molecular Neuroscience 08/2013; 51(3). DOI:10.1007/s12031-013-0080-y · 2.76 Impact Factor
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    ABSTRACT: Microtubule-associated protein tau is found to be accumulated and aggregated in the brains of individuals with Alzheimer's disease and related tauopathies. Dual-specificity tyrosine-phosphorylation regulated kinase 1A (Dyrk1A) is overexpressed in Down syndrome and may play a critical role in the early onset of tau pathology in this disease. To investigate the effect of Dyrk1A on tau expression, we co-expressed different isoforms of tau with Dyrk1A in HEK-293FT cells and measured the mRNA and protein levels of tau using RT-PCR and western blots, respectively. We further investigated the mechanism of regulation of tau expression by Dyrk1A. We found that Dyrk1A enhanced tau expression in a dose-dependent manner. The enhancement did not require the kinase activity of Dyrk1A. Dyrk1A increased the expression of tau isoforms containing exon 10 to a larger extent than isoforms lacking exon 10. The expression of endogenous tau in neuronal cells was also regulated by Dyrk1A, and increased tau levels were found in the brains of Ts65Dn mice that overexpress Dyrk1A due to partial trisomy of chromosome 16. Dyrk1A did not enhance tau gene transcription, but increased tau mRNA stability. These results suggest that Dyrk1A enhances tau expression by stabilizing its mRNA and provides a novel insight into the regulation of tau expression and a molecular mechanism of tauopathies.
    Journal of Alzheimer's disease: JAD 07/2013; 37(3). DOI:10.3233/JAD-130824 · 4.15 Impact Factor
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    ABSTRACT: Nuclear factor of activated T-cells, cytoplasmic 4 (NFATc4), a transcriptional factor, is involved in the control about the flow of genetic information and the modulation of diverse cellular activities. Accumulating evidence has demonstrated that NFATc4 exerted a pro-apoptotic effect in multiple diseases. Here, we explored the NFATc4's roles during the pathophysiological processes of intracerebral hemorrhage (ICH). An ICH rat model was built and evaluated according to behavioral testing. Using Western blot, immunohistochemistry, and immunofluorescence, significant up-regulation of NFATc4 was found in neurons in brain areas surrounding the hematoma following ICH. Increasing NFATc4 expression was found to be accompanied by the up-regulation of Fas ligand (FasL), active caspase-8, and active caspase-3, respectively. Besides, NFATc4 co-localized with active caspase-3 in neurons, indicating its role in neuronal apoptosis. Our in vitro study, using NFATc4 RNA interference in PC12 cells, further confirmed that NFATc4 might exert its pro-apoptotic function in neuronal apoptosis through extrinsic pathway. Thus, NFATc4 may play a role in promoting the brain secondary damage following ICH.
    Cellular and Molecular Neurobiology 07/2013; 33(7). DOI:10.1007/s10571-013-9955-2 · 2.20 Impact Factor
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    ABSTRACT: SGTB (Small glutamine-rich tetratricopeptide repeat (TPR)-containing, β) plays a critical role in protein-protein interactions. The interaction between SGTB and heat shock cognate protein (Hsc70)/heat shock protein (Hsp70) has aroused much attention in recent years. The present study was designed to elucidate dynamic changes in SGTB expression and distribution in the cerebral cortex in a lipopolysaccharide (LPS)-induced neuroinflammation rat model. It was found that SGTB expression was increased significantly in apoptotic neurons after LPS injection. The result of our in vitro study suggested that SGTB up-regulation might be associated with neuronal apoptosis after H2O2 challenge. In addition, silencing of SGTB in cultured PC12 (Pheochromocytoma) by siRNA indicated that SGTB was required for neuronal apoptosis induced by oxidative stress. Our finding about the cellular signal pathway may provide a new strategy against neuronal apoptosis in neuroinflammation in CNS.
    Journal of molecular histology 07/2013; 44(5). DOI:10.1007/s10735-013-9517-4 · 1.98 Impact Factor
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    ABSTRACT: Chronic administration of D-galactose (D-gal) is widely used to mimic the process of brain aging; however, the neural mechanisms are still poorly understood. In this study, we investigated the effect of long-term D-gal treatment on the number of GABA-immunoreactive neurons in rat cerebral cortex and the behavioral correlates. After eight weeks of daily subcutaneous injection of D-gal (100mg/ml/kg), rats showed reduced exploratory activity and lower ambulation in the open field compared to controls. There was no significant reduction in total neurons in the cortex, but there was a marked decrease in the number of GABA-immunoreactive neurons in all cortical layers of D-gal-treated rats. The ratio of GABA-immunoreactive neurons to total neurons was significantly lower in all cortical layers of D-gal-treated rats, with greatest reductions in output layers III (39.9% reduction), V (46.3%), and VI (48.4%). Our study provides the first evidence that chronic D-gal treatment may decrease cortical GABAergic neurotransmission, especially in cerebral output layers. The reduction in GABA-immunoreactive cell number likely disrupts the intracortical excitatory/inhibitory balance and may contribute to the behavioral deficits observed in this aging model.
    Neuroscience Letters 06/2013; DOI:10.1016/j.neulet.2013.06.021 · 2.06 Impact Factor
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    ABSTRACT: Bnip3L, also known as NIX, is a homolog of the E1B 19K/Bcl-2 binding and pro-apoptotic protein Bnip3 which can bind to Bcl-2 to elaborate that effect. In tumor cells, Bnip3L played a role in tumor growth inhibition, but some studies argued hypoxia-induced autophagy via Bnip3L was a survival mechanism that promoted tumor progression. In heart muscle, it related to decreased myocardial function. However, its function in intracerebral hemorrhage (ICH) is still not clear. In this frame, we found the Bnip3L expression increased in the perihematomal region in adult rats after performed ICH. Double immunofluorenscence staining manifested that Bnip3L co-located with neurons, not astrocytes or oligodendrocytes. Furthermore, we detected that neuronal apoptosis marker active caspase-3 had colocalizations with Bnip3L. In addition, colocalizations and co-immunoprecipitation between Bnip3L and Bcl-2, consistent with previous study, were also found. All our findings suggested that Bnip3L might be involved in the pathophysiology of ICH.
    Journal of molecular histology 06/2013; 44(5). DOI:10.1007/s10735-013-9506-7 · 1.98 Impact Factor
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    ABSTRACT: Traumatic brain injury (TBI) triggers a complex series of neurochemical and signaling changes that lead to neuronal dysfunction and overreactive astrocytes. In the current study, we showed that interactions between SCYL1-bp1 and Pirh2 are involved in central nervous system (CNS) injury and repair. Western blot and immunohistochemical analysis of an acute traumatic brain injury model in adult rats revealed significantly increased levels of SCYL1-bp1 and Pirh2 in the ipsilateral brain cortex, compared to contralateral cerebral cortex. Immunofluorescence double-labeling analyses further revealed that SCYL1-bp1 is mainly co-expressed with NeuN. Terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling staining data supported the involvement of SCYL1-bp1 and Pirh2 in neuronal apoptosis after brain injury. We additionally examined the expression profiles of active caspase-3, which were altered in correlation with the levels of SCYL1-bp1 and Pirh2. Notably, both SCYL1-bp1 and Pirh2 were colocalized with active caspase-3, and all three proteins participated in neuronal apoptosis. Immunoprecipitation experiments further revealed interactions of these proteins with each other in the pathophysiology process. To our knowledge, this is the first study to report interactions between SCYL1-bp1 and Pirh2 in traumatic brain. Our data collectively indicate that SCYL1-bp1 and Pirh2 play important roles in CNS pathophysiology after TBI.
    Journal of molecular histology 03/2013; DOI:10.1007/s10735-013-9488-5 · 1.98 Impact Factor
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    ABSTRACT: αB-crystallin (αBC) is involved in diverse cellular activities. Previous studies demonstrated that αBC had anti-apoptotic and proliferation-promoting effects in multiple diseases. Here, we explored the αBC's roles in the pathophysiology of intracerebral hemorrhage (ICH). An ICH rat model was established and assessed by behavioral tests. Using Western blot and immunohistochemistry, significant up-regulation of αBC was found in neurons and astrocytes in brain areas surrounding the hematoma following ICH. Increase of αBC expression was found to be accompanied by the increased expression of proliferating cell nuclear antigen (PCNA), p53, Bax, and active-caspase-3. αBC was co-localized with PCNA in astrocytes or active-caspase-3 in neurons, suggesting its role in astrocyte proliferation and neuronal apoptosis. Our in vitro study, using αBC RNA interference in PC12 cells, indicated that αBC might exert its anti-apoptotic function in neuronal apoptosis. Thus, αBC may play a role in protecting the brain from secondary damage following ICH.
    Journal of Molecular Neuroscience 02/2013; 51(1). DOI:10.1007/s12031-013-9970-2 · 2.76 Impact Factor
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    ABSTRACT: Ras homolog enriched in the brain (Rheb) is a homolog of Ras GTPase that regulates cell growth, proliferation, and cell cycle via mammalian target of rapamycin (mTOR). Recently, it has been confirmed that Rheb activation not only promotes cellular proliferation and differentiation but also enhances cellular apoptosis in response to diverse toxic stimuli. However, the function of Rheb in the central nervous system (CNS) is still with limited understanding. To elaborate whether Rheb was involved in CNS injury, we performed a neuroinflammatory model by lipopolysaccharide (LPS) lateral ventral injection in adult rats. Upregulation of Rheb was observed in the brain cortex by performing western blotting and immunohistochemistry. Double immunofluorescent staining demonstrated that Rheb was mainly in active astrocytes and neurons. PCNA and active caspase-3 were upregulated, and co-labeling with Rheb, which indicated that Rheb might be relevant to astrocytic proliferation and neuronal apoptosis following the inflammatory response by LPS-induced. Furthermore, we also found that the expression profiles of cyclinD1 and CDK4 were parallel with that of Rheb in a time-space dependent manner. Finally, knocking down Rheb by siRNA and treatment with rapamycin or lovastatin showed that not only astrocytic proliferation decreased but also neuronal protection. Based on our data, we suggested that Rheb might play an important role in physiological and pathological functions following neuroinflammation caused by LPS, which might provide a potential target to the treatment of neuroinflammation.
    Neurochemistry International 02/2013; 62(4). DOI:10.1016/j.neuint.2013.01.025 · 2.65 Impact Factor
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    ABSTRACT: CBLL1 (Casitas B-lineage lymphoma-transforming sequence-like protein 1) also known as Hakai, was originally identified as an E3 ubiquitin-ligase for the E-cadherin complex. Recent data have provided evidences for novel biological functional role of CBLL1 during tumor progression and other diseases. However, its distribution and function in the central nervous system (CNS) remains unclear. In this study, we found CBLL1 was significant up-regulation in cerebral cortex after LPS administration and immunofluorescent labeling indicated that CBLL1 was localized striking in the neurons. We also investigated co-staining of CBLL1 and active-caspase-3 and cyclin D1 in the cerebral cortex following LPS administration. Based on our data, we speculated that CBLL1 might play an important role in neuronal apoptosis following LPS administration and might provide a basis for the further study on its role in cell cycle re-entry in neuroinflammation in CNS.
    Journal of molecular histology 11/2012; DOI:10.1007/s10735-012-9467-2 · 1.98 Impact Factor
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    ABSTRACT: SKIP (Ski-interacting protein), is part of nuclear regulatory complexes and interacts with factors involved in preinitiation, splicing and polyadenylation, potentiates the activity of important transcription factors, involved in an increasing number of signaling cascades. However, its distribution and function in the central nervous system remains poorly understood. In this study, western blot analysis, RT-PCR and immunohistochemistry showed a significant up-regulation of SKIP in ipsilateral peritrauma cortex compared with the sham group. Immunofluorescent labeling indicated that SKIP was localized striking in the neurons, but not astrocytes and oligodendrocytes; co-localization of SKIP and active caspase-3 and PCNA in the ipsilateral cortex. In addition, the expression patterns of active caspase-3 and PCNA were parallel with that of SKIP. Based on our data, we speculated that SKIP might play an important role in neuronal apoptosis following TBI; and might provide a basis for the further study on its role in cell cycle re-entry in traumatic brain injury.
    Journal of molecular histology 09/2012; 44(1). DOI:10.1007/s10735-012-9444-9 · 1.98 Impact Factor
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    ABSTRACT: BAG-1 protein was initially identified as a Bcl-2-binding protein. It was reported to enhance Bcl-2 protection from cell death, suggesting that BAG-1 represents a new type of anti-cell death gene. Moreover, recent study has shown that BAG-1 can enhance the proliferation of neuronal precursor cells, attenuate the growth inhibition induced by siah1. However, its function and expression in the central nervous system lesion are not been understood very well. In this study, we performed a traumatic brain injury (TBI) model in adult rats and investigated the dynamic changes of BAG-1 expression in the brain cortex. Double immunofluorescence staining revealed that BAG-1 was co-expressed with NEURON and glial fibrillary acidic protein (GFAP). In addition, we detected that proliferating cell nuclear antigen had the co-localization with GFAP, and BAG-1. All our findings suggested that BAG-1 might involve in the pathophysiology of brain after TBI.
    Journal of molecular histology 04/2012; 43(3):335-42. DOI:10.1007/s10735-012-9408-0 · 1.98 Impact Factor