PNAS：干细胞在幼年个体而非成年个体中分化为心脏细胞

近日，来自康奈尔大学和伯恩大学的研究者研究指出，在人们早年时心脏病发作后，干细胞实际上可以取代坏死的心脏组织，但是这些干细胞在人成年后会丧失再生的能力。这项研究中，研究者使用小鼠作为研究模型发现未分化的前体细胞在两天大的小鼠体内可以分化为心脏细胞，但是在成体小鼠中却不行。

目前在成年个体中是否存在未分化的前体干细胞仍存在争议，如果在成年个体中确实存在有能力的干细胞，为何在个体梗塞之后没有新的心脏细胞呢？是否这取决于干细胞的缺少或者是梗塞可以抑制干细胞形成新的心脏细胞，目前这仍然是一个问题。研究者Michae这样说，研究者的相关研究成果将于8月29日刊登在国际杂志PNAS上。

研究者Kotlikoff和其同事发现两天大的小鼠可以产生新的心脏细胞，而且几乎可以完全从梗死中恢复过来，这就证明了损伤并不能抑制干细胞发育为心脏细胞。相同的实验也在成年小鼠中进行，可是并没有产生新的心脏细胞，证实了成年个体没有必要的干细胞来产生新的心脏细胞，尽管干细胞可以产生新的血管细胞。

在成年小鼠心脏中发现的干细胞丧失了发育为心脏细胞的能力，仅仅具有发育为血管的能力。研究者的相关研究由国立卫生研究院提供支持。

编译自：Stem Cells Repair Hearts Early in Life, but Not in Adults

doi:10.1073/pnas.1208114109
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c-kit+ precursors support postinfarction myogenesis in the neonatal, but not adult, heart

Sophy A. Jestya,1,2, Michele A. Steffeya,2,3, Frank K. Leea,2, Martin Breitbachb, Michael Hesseb, Shaun Reininga, Jane C. Leea, Robert M. Dorana, Alexander Yu. Nikitina, Bernd K. Fleischmannb,4, and Michael I. Kotlikoffa,4

We examined the myogenic response to infarction in neonatal and adult mice to determine the role of c-kit+ cardiovascular precursor cells (CPC) that are known to be present in early heart development. Infarction of postnatal day 1–3 c-kitBAC-EGFP mouse hearts induced the localized expansion of (c-kit)EGFP+ cells within the infarct, expression of the c-kit and Nkx2.5 mRNA, myogenesis, and partial regeneration of the infarction, with (c-kit)EGFP+ cells adopting myogenic and vascular fates. Conversely, infarction of adult mice resulted in a modest induction of (c-kit)EGFP+ cells within the infarct, which did not express Nkx2.5 or undergo myogenic differentiation, but adopted a vascular fate within the infarction, indicating a lack of authentic CPC. Explantation of infarcted neonatal and adult heart tissue to scid mice, and adoptive transfer of labeled bone marrow, confirmed the cardiac source of myogenic (neonate) and angiogenic (neonate and adult) cells. FACS-purified (c-kit)EGFP+/(αMHC)mCherry− (noncardiac) cells from microdissected infarcts within 6 h of infarction underwent cardiac differentiation, forming spontaneously beating myocytes in vitro; cre/LoxP fate mapping identified a noncardiac population of (c-kit)EGFP+ myocytes within infarctions, indicating that the induction of undifferentiated precursors contributes to localized myogenesis. Thus, adult postinfarct myogenic failure is likely not due to a context-dependent restriction of precursor differentiation, and c-kit induction following injury of the adult heart does not define precursor status.