以前的研究認(rèn)為,，細(xì)胞衰老是一種腫瘤抑制機(jī)制，但除了癌癥之外,，很少有研究探索細(xì)胞衰老在其他疾病中的作用?，F(xiàn)在，研究人員提出,，受蛋白質(zhì)CCN1調(diào)控的細(xì)胞衰老可預(yù)防受傷期間過多組織的形成,，即組織纖維變性。
>>>借著上海世博會(huì)的良好契機(jī),，"第一屆腫瘤基礎(chǔ)和轉(zhuǎn)化醫(yī)學(xué)國(guó)際研討會(huì)"將于2010年10月12日在中國(guó)上海盛大開幕,，這將為廣大活躍在腫瘤基礎(chǔ)和轉(zhuǎn)化醫(yī)學(xué)第一線的科研工作者提供一個(gè)互動(dòng)交流的平臺(tái)。
會(huì)議官方網(wǎng)站：www.cancerasia.org
細(xì)胞衰老是指細(xì)胞保持存態(tài)但失去再分化能力的狀態(tài),。肉芽組織是傷口愈合期間所形成的一種軟組織聯(lián)接,。Jun和Lau發(fā)現(xiàn)，衰老的細(xì)胞出現(xiàn)在小鼠的肉芽組織中,。缺失CCN1功能的小鼠只出現(xiàn)了更少的衰老細(xì)胞,。他們因此得出結(jié)論認(rèn)為，CCN1調(diào)控了細(xì)胞的衰老機(jī)制,，并通過CCN1功能的插入來鑒別這種機(jī)制,。
他們還發(fā)現(xiàn),，缺失CCN1的小鼠，在其傷口愈合期間會(huì)出現(xiàn)更多的組織纖維變性,。相反,，將CCN1插入受傷的組織會(huì)導(dǎo)致細(xì)胞衰老，從而預(yù)防纖維化組織的出現(xiàn),。組織纖維化與多種疾病有關(guān),，新數(shù)據(jù)支持了細(xì)胞衰老在抗纖維化機(jī)制中的重要作用。(生物谷Bioon.net)
生物谷推薦原文出處：
Nature Cell Biology doi:10.1038/ncb2070
The matricellular protein CCN1 induces fibroblast senescence and restricts fibrosis in cutaneous wound healing
Joon-Il Jun1 & Lester F. Lau1
Cellular senescence is a recognized mechanism of tumour suppression; however, its contribution to other pathologies is not well understood. We show that the matricellular protein CCN1 (also known as CYR61; cysteine-rich protein 61), which is dynamically expressed at sites of wound repair, can induce fibroblast senescence by binding to integrin α6β1 and the heparan sulphate proteoglycans (receptors involved in cell adhesion). CCN1 induces DNA damage response pathways and activates p53 and the RAC1–NOX1 complex, which generates reactive oxygen species (ROS). This results in the ROS-dependent activation of the p16INK4a/pRb pathway, leading to senescence and concomitant expression of antifibrotic genes. Senescent fibroblasts accumulate in granulation tissues of healing cutaneous wounds and express antifibrotic genes in wild-type mice. These processes are lost in knockin mice that express a senescence-defective Ccn1 mutant, resulting in exacerbated fibrosis. Topical application of CCN1 protein to wounds reverses these defects. Thus, fibroblast senescence is a CCN1-dependent wound healing response in cutaneous injury that functions to curb fibrosis during tissue repair.
