係research角度其實都幾亂下
一大原因就係"mesenchymal stem cell"呢個term 以及"msc"呢個簡稱用得好差
宜家一般共識係佢未算stem cell (lack of proof of long term self renewal)
更大問題連"what is msc"都係各有各講
唔同studies隨時睇緊唔同嘅population
可能用緊cells from different organ of origin (bone marrow/adipose tissue/umbilical cord/muscle/etc)
有唔同嘅isolation strategies
但係全部都話自己係msc 唔亂就奇
:^(
Still msc is known to be multipotent progenitor(我supervisor 立場係叫佢做multipotent/mesenchymal stromal cell)
即係可以變adipocyte/fibroblast/osteocyte/chondrocyte
(btw fibroblast in this context≈scar forming cell)
但係真係打落關節後佢會變咩就要睇兩樣野
一係intrinsic factor
即係個cell本身會唔會already partly committed to adipogenesis/fibrogenesis/etc?
近年single cell rna sequencing in msc就搵到唔同subpopulations
簡單咁講即係其實有msc "type"1/2/3/4/...
可能type 1就係特別鍾意變adipocytes
type 2特別鍾意變osteocytes (9up example only)
咁你打左呢幾種落關節仲唔瀨野？
另外就要睇local environment (ie "niche")
附近嘅cell produce左咩factors 甚至係physical property (elastic modulus/viscoelasticity)都會影響到cell fate commitment
特別係傷緊發炎緊嘅會只會更加亂
假設真係有某msc subtype within svf can specifically give rise to chondrocyte
單靠centrifugation physically isolate fat-derived msc
無select against唔關事嘅cell 又無enrich你真正需要個population
實際效果有幾多呢