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Endoplasmic reticulum stress induced by tunicamycin and antagonistic effect of Tiantai No.1 (天泰1号) on mesenchymal stem cells
Endoplasmic reticulum stress induced by tunicamycin and antagonistic effect of Tiantai No.1 (天泰1号) on mesenchymal stem cells
- 中国结合医学杂志（英文版） 2010年16卷第1期 页码：41-49
- Affiliations：
1. Shenzhen Hospital of Southern Medical University,Guangdong Province,Shenzhen,China
2. Larry Hillblom Islet Research Center, David Geffen School of Medicine, UCLA,Los Angeles,USA
- Author bio：
- Funds：Supported by the National Foundation of Traditional Chinese Medical Science and Technology (No. 02-03LP41);Key Project of the Foundation of Science and Technology of Guangdong Province (No. 2006B35630007)
DOI：10.1007/s11655-010-0041-z
中图分类号：纸质出版日期：2010，
网络出版日期：2010-2-4，
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Wu, Zz., Li, Yh., Huang, A.C.J. et al. Endoplasmic reticulum stress induced by tunicamycin and antagonistic effect of Tiantai No.1 (天泰1号) on mesenchymal stem cells., Chin. J. Integr. Med. 16, 41–49 (2010). https://doi.org/10.1007/s11655-010-0041-z
Zheng-zhi Wu, Ying-hong Li, Andrew C. J. Huang, et al. Endoplasmic reticulum stress induced by tunicamycin and antagonistic effect of Tiantai No.1 (天泰1号) on mesenchymal stem cells[J]. Chinese Journal of Integrative Medicine, 2010,16(1):41-49.
Wu, Zz., Li, Yh., Huang, A.C.J. et al. Endoplasmic reticulum stress induced by tunicamycin and antagonistic effect of Tiantai No.1 (天泰1号) on mesenchymal stem cells., Chin. J. Integr. Med. 16, 41–49 (2010). https://doi.org/10.1007/s11655-010-0041-z DOI：
Zheng-zhi Wu, Ying-hong Li, Andrew C. J. Huang, et al. Endoplasmic reticulum stress induced by tunicamycin and antagonistic effect of Tiantai No.1 (天泰1号) on mesenchymal stem cells[J]. Chinese Journal of Integrative Medicine, 2010,16(1):41-49. DOI： 10.1007/s11655-010-0041-z.
摘要
Changes of the internal and external cellular environments can induce calcium homeostasis disorder and unfolded protein aggregation in the endoplasmic reticulum (ER). This ER function disorder is called endoplasmic reticulum stress (ERS). Severe long-term ERS can trigger the ER apoptosis signaling pathway
resulting in cell apoptosis and organism injury. Recent researches revealed that ERS-induced cell death was involved in the neurocyte retrogradation in the progress of neuron degenerative diseases
such as Alzheimer’s disease (AD)
Parkinson’s disease and so on. Therefore
the protection effect of the traditional Chinese drug—Tiantai No. 1 (天泰1号) on the ERS injury of AD was investigated at the molecular gene level in this study with a view to explore the gene pharmacodynamic actions and mechanisms of this drug. Primarily cultured marrow mesenchymal stem cells (MSCs) of rats were treated by tunicamycin (TM) in order to induce ERS. RT-PCR
fluorescence immunocytochemistry and Western blot techniques were used to determine the mRNA and protein expression levels of the protective stress protein-ER molecular chaperones GRP78 and GRP94 (which would assist cells to resist cellular stress injury)
and to determine the mRNA and protein expression levels of apoptosis promoting molecule Caspase-12 on the membrane of the ER
respectively. Protein expression levels of GRP78 and GRP94 were significantly increased in the TM-induced MSCs
and the mRNA level of Caspase-12 was also remarkably increased in the TM-induced MSCs (P<0.05). All these proved that the ERS model was successfully established by TM in MSC. Meanwhile
the mRNA and protein levels of GRP78 and GRP94 were all significantly increased compared with the model group (P<0.05 or P<0.01) after MSCs were treated with Tiantai No.1 while the mRNA and protein expression levels of Caspase-12 were significantly decreased compared with the model group (P<0.05 or P<0.01). This effect showed a dose dependent manner. Tiantai No.1 might attenuate the cell apoptosis induced by ERS injury
and thus protect the neurons against AD.
Abstract
Changes of the internal and external cellular environments can induce calcium homeostasis disorder and unfolded protein aggregation in the endoplasmic reticulum (ER). This ER function disorder is called endoplasmic reticulum stress (ERS). Severe long-term ERS can trigger the ER apoptosis signaling pathway
resulting in cell apoptosis and organism injury. Recent researches revealed that ERS-induced cell death was involved in the neurocyte retrogradation in the progress of neuron degenerative diseases
such as Alzheimer’s disease (AD)
Parkinson’s disease and so on. Therefore
the protection effect of the traditional Chinese drug—Tiantai No. 1 (天泰1号) on the ERS injury of AD was investigated at the molecular gene level in this study with a view to explore the gene pharmacodynamic actions and mechanisms of this drug. Primarily cultured marrow mesenchymal stem cells (MSCs) of rats were treated by tunicamycin (TM) in order to induce ERS. RT-PCR
fluorescence immunocytochemistry and Western blot techniques were used to determine the mRNA and protein expression levels of the protective stress protein-ER molecular chaperones GRP78 and GRP94 (which would assist cells to resist cellular stress injury)
and to determine the mRNA and protein expression levels of apoptosis promoting molecule Caspase-12 on the membrane of the ER
respectively. Protein expression levels of GRP78 and GRP94 were significantly increased in the TM-induced MSCs
and the mRNA level of Caspase-12 was also remarkably increased in the TM-induced MSCs (P<0.05). All these proved that the ERS model was successfully established by TM in MSC. Meanwhile
the mRNA and protein levels of GRP78 and GRP94 were all significantly increased compared with the model group (P<0.05 or P<0.01) after MSCs were treated with Tiantai No.1 while the mRNA and protein expression levels of Caspase-12 were significantly decreased compared with the model group (P<0.05 or P<0.01). This effect showed a dose dependent manner. Tiantai No.1 might attenuate the cell apoptosis induced by ERS injury
and thus protect the neurons against AD.
关键词
endoplasmic reticulum stressAlzheimer’s diseasemesenchymal stem celltunicamycinTiantai No.1
Keywords
endoplasmic reticulum stressAlzheimer’s diseasemesenchymal stem celltunicamycinTiantai No.1
references
Lin L, Tang CS, Yuan WJ. Endoplasmic reticulum stress. Prog Physiol Sci (Chin) 2003;34:333–335.
Imaizumi K, Tohyama M. The regulation of unfolded protein response by OASIS, a transmembrane bZIP transcription factor, in astrocytes. Nippon Yakurigaku Zasshi 2004;124:383–390.
Ferri KF, Kroemer G. Organelle-specific initiation of cell death pathways. Nat Cell Biol 2001;3:E255–E263.
Ma Y, Hendershot LM. The role of the unfolded protein response in tumour development: friend or foe? Nat Rev Cancer 2004;4:966–977.
Li ZQ, Zhou AR, Tang CS. Molecular mechanism on endoplasmic reticulum stress responses. Chin J Biochem Mol Biol (Chin) 2004;20:283–288.
Breckenridge DG, Germain M, Mathai JP, Nguyen M, Shore GC. Regulation of apoptosis by endoplasmic reticulum pathways. Oncogene 2003;22:8608–8618.
Liu H, Miller E, van de Water B, Stevens JL. Endoplasmic reticulum stress proteins block oxidantinduced Ca2+ increases and cell death. J Biol Chem 1998;273:12858–12862.
Zhang PL, Lun M, Teng J, Huang J, Blasick TM, Yin L, et al. Preinduced molecular chaperones in the endoplasmic reticulum protect cardiomyocytes from lethal injury. Ann Clin Lab Sci 2004;34:449–457.
Xu CY, Bailly-Maitre B, Reed JC. Endoplasmic reticulum stress: cell life and death decisions. J Clin Invest 2005;115:2656–2664.
Hu P, Han Z, Couvillon AD, Exton JH. Critical role of endogenous Akt/IAPs and MEK1/ERK pathways in counteracting ER stress-induced cell death. J Biol Chem 2004;279:49420–49429.
Verkhratsky A, Toescu EC. Endoplasmic reticulum Ca2+ homoestasis and neuronal death. J Cell Mol Med 2003;7:351–361.
Geula C, Wu CK, Saroff D, Lorenzo A, Yuan M, Yanker BA. Aging renders the brain vulnerable to amyloid-beta-protein neurotoxicity. Nat Med 1998;4:827–831.
Chu K, Jung KH, Kim SJ, Lee ST, Kim J, Park HK, et al. Transplantation of human neural stem cells protect against ischemia in a preventive mode via hypoxia-inducible factor-1 alpha stabilization in the host brain. Brain Res 2008;1207C:182–192.
Miller FD. Riding the waves: neural and nonneural origins for mesenchymal stem cells. Cell Stem Cell 2007;1:129–130.
Whittemore SR, Zhang YP, Shields CB, Magnuson DS. Optimizing stem cell grafting into the CNS. Methods Mol Biol 2008;438:375–382.
Newman MB, Bakay RA. Therapeutic potentials of human embryonic stem cells in Parkinson’s disease. Neurotherapeutics 2008;5:237–251.
Sugaya K, Alvarez A, Marutle A, Kwak YD, Choumkina E. Stem cell strategies for Alzheimer’s disease therapy. Panminerva Med 2006;48:87–96.
Biorklund A, Lindvatll O. Cell replacement therapies for central nervous system disorder. Nat Neurosci 2000;3:537–544.
Chai LH, Wu SX, Yan WH, Ma YF. Human bone marrow mesenchymal stem cells differentiated into dopaminergenic neurons in vitro. Chin J Biotechnol (Chin) 2007;23:252–256.
Sotiropoulou PA, Papamichail M. Immune properties of mesenchymal stem cells. Methods Mol Biol 2007;407:225–243.
Sensebe L. Clinical grade production of mesenchymal stem cells. Biomed Mater Engl 2008;18(1 Suppl):S3–10.
Singh S, Joned BJ, Crawford R, Xiao Y. Characterization of a mesenchymal-like stem cell population from osteophyte tissue. Stem Cells Dev 2008;17:245–254.
Hosseinkhani H, Hosseinkhani M, Kobayashi H. Proliferation and differentiation of mesenchymal stem cells using self-assembled peptide amphiphile nanofibers. Biomed Mater 2006;1:8–15.
Wang L, Li Y, Lu DY. Neurotrophins promote bone marrow stromal cells (MSCs) to express neural proteins in vitro. Stroke 2001;32:334.
Sanchez RJ, Song S, Cardozo PF, Hazzi C, Stedeford T, Willing A, et al. Adult bone marrow stromal cells differentiate into neural cells in vitro. Exp Neurol 2000;164:247–256.
Wu ZZ, Li M, Li YF, Zhang YF. Effects of Tiantai No.1 on relative neuropeptides of spontaneous aged dementia mice. Neuroscience Bull 2004;20:167–170.
Wu ZZ, Li YH, Li M, Zhang YP, Jia XQ, Chen MY. Influence of Buganyangshui recipe on synaptic plasticity of the hippocampal CA1 region of spontaneous Alzheimer disease models: Quantitative research of ultrastructure. Chin J Tradit Med Sci Technol (Chin) 2007;14:444–446.
Wu ZZ, Li M, Li YF, Zhang YF, Jia XQ, Chen MY. Quantitative study of Tiantai No. 1 on superoxidative dismutase and lipofuscin in relevant cerebral areas of spontaneous Alzheimer disease in mice. Chin J Clin Rehabil (Chin) 2005;9:178–181.
Woodbury D, Sehwarz EJ, Prockop DJ, Black IB. Adult rat and human bone marrow stromal cells differentiate into neurous. J Nourosci Res 2000;61:364–370.
Seshareddy K, Troyer D, Weiss ML. Method to isolate mesenchymal-like cells from Wharton’s Jelly of umbilical Cord. Methods Cell Biol 2008;86:101–119.
Zhang GP, Li YY, Lu JC, Ou HJ. Ursolic acid induces apoptosis through effects on Bax and Bcl-2 expression in human MCF-7 cells. J Fourth Military Med Univ 2005;26:1877–1880.
Chen KJ, Lu AP. From Chinese version of integrative medicine to globalized integrative medicine: Impression on the 3rd World Integrative Medicine Congress. Chin J Integr Med 2007;13:244–245.
Wang XM, Fu H, Liu GX, Zhu W, Li L, Yang JX. Effect of modified Wuzi Yanzong Granule on patients with mild cognitive impairment from oxidative damage aspect. Chin J lntegr Med 2007;13:258–263.
Wang XM, Fu H, Liu GX, Song P, Tu PF, Wang YH. Clinical study on treatment of mild cognitive impairment by modified Wuzi Yanzong Granule. Chin J Integr Tradit West Med (Chin) 2004;24:392–395.
Harding HP, Zhang Y, Ron D. Protein translation and folding are coupled by an endoplasmic-reticulum-resident kinase. Nature 1999;397:271–274.
Sato N, Imaizumi K, Manabe T, Taniguchi M, Hitomi J, Katayama T, et al. Increased production of beta-amyloid and vulnerability to endoplasmic reticulum stress by an aberrant spliced form of presenilin-2. J Biol Chem 2001;276:2108–2114.
Imai Y, Soda M, Takahashi R. Parkin suppresses unfolded protein stress-induced cell death through its E3 ubiquitin-protein ligase activity. J Biol Chem 2000;275:35661–35664.
Imai Y, Soda M, Inoue H, Hattori N, Mizuno Y, Takahashi R. An unfolded putative transmembrane polypeptide, which can lead to endoplasmic reticulum stress, is a substrate of Parkin. Cell 2001;105:891–902.
Imaizumi K, Miyoshi K, Katayama T, Yoneda T, Taniguchi M, Kudo T, et al. The unfolded protein response and Alzheimer’s disease. Biophys Biochem Acta 2001;1536:85–96.
Imaizumi K, Katayama T, Tohyama M. Presenilin and UPR. Nat Cell Biol 2001;3:E104.
Katayama T, Imatzumi K, Sate N, Miyoshi K, Kudo T, Hitomi J, et al. Presenilin-1 mutations down-regulate the signaling pathway of the unfolded-protein response. Nat Cell Biol 1999;1:479–485.
Katayama T, Imaizumi K, Manabe T, Hitomi J, Kudo T, Tohyama M. Induction of neuronal death by ER stress in Alzheimer’s disease. J Chem Neuroanat 2004;28:67–78.
Park IH, Arora N, Huo H, Maherali N, Ahfeldt T, Shimamura A, et al. Disease-specific induced pluripotent stem cells. Cell 2008;134:877–886.
Li YH, Wu ZZ, Wu WK, Li M, Wang JG, Yang M, et al. Rat mesenchymal stem cells oriented differentiation into neuron-like cells induced by natural cerebrolysin. Chin J Pathophysiol (Chin) 2009;25:1548–1553.
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