TAILIEUCHUNG - Báo cáo khoa học: Expression and secretion of interleukin-1b, tumour necrosis factor-a and interleukin-10 by hypoxia- and serum-deprivation-stimulated mesenchymal stem cells Implications for their paracrine roles

To understand the potential paracrine roles of interleukin-1b (IL-1b), tumour necrosis factor-a(TNF-a) and interleukin-10 (IL-10), the expres-sion and secretion of these factors by rat bone marrow-derived mesenchy-mal cells stimulated by hypoxia (4% oxygen) and serum deprivation (hypoxia⁄SD) were investigated. | Expression and secretion of interleukin-1 b tumour necrosis factor-a and interleukin-10 by hypoxia- and serum-deprivation-stimulated mesenchymal stem cells Implications for their paracrine roles Zongwei Li Hua Wei Linzi Deng Xiangfeng Cong and Xi Chen Research Center for Cardiac Regenerative Medicine Chinese Academy of MedicalSciences Peking Union MedicalCollege Beijing China Keywords IL-10 IL-1 b mesenchymalstem cell paracrine TNF-a Correspondence X. Chen X. Cong Research Center for Cardiac Regenerative Medicine The Ministry of Health Cardiovascular Institute Fu Wai Hospital Chinese Academy of MedicalSciences Peking Union Medical College 167 Beilishilu Beijing 100037 China Fax Tel 86 10 88398584 E-mail chenxifw@ xiangfeng_cong@ Received 26 April 2010 revised 27 June 2010 accepted 10 July 2010 doi To understand the potential paracrine roles of interleukin-1 b IL-1b tumour necrosis factor-a TNF-a and interleukin-10 IL-10 the expression and secretion of these factors by rat bone marrow-derived mesenchymal cells stimulated by hypoxia 4 oxygen and serum deprivation hypoxia SD were investigated. We found that hypoxia SD induced nuclear factor kappa Bp65-dependent IL-1b and TNF-a transcription. Furthermore hypoxia SD stimulated the translation of pro-IL-1b and its processing to mature IL-1b although the translation of TNF-a was unchanged. Unexpectedly the release of IL-1b and TNF-a from hypox-ia SD-stimulated mesenchymal cells was undetectable unless ATP or lipopolysaccharide was present. This result suggests that IL-1b and TNF-a are not responsible for the paracrine effects of mesenchymal cells under ischaemic conditions. We also found that hypoxia SD induced the transcription and secretion of IL-10 which were significantly enhanced by lipopolysaccharide and the proteasomal inhibitor MG132. Moreover both the conditioned medium from hypoxia SD-stimulated mesenchymal cells MSC-CM and IL-10 efficiently inhibited .

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