Why grow soft?

科學(xué)家一直都在研究用天然的或者合成的基質(zhì)環(huán)境來培養(yǎng)細(xì)胞，從而能誘導(dǎo)細(xì)胞呈現(xiàn)應(yīng)有的形態(tài)，這是在剛性的培養(yǎng)材質(zhì)上是做不到的。不幸的是，讓細(xì)胞生長在柔軟的基質(zhì)里或基質(zhì)表面不僅價(jià)格昂貴，而且是很不切實(shí)際的。

Softwell克服了這些挑戰(zhàn)。它可以讓您的研究在柔軟的環(huán)境下細(xì)胞的行為。進(jìn)一步講，它提供了不同柔軟度的環(huán)境，引導(dǎo)您發(fā)現(xiàn)不同類型細(xì)胞的形態(tài)，可以進(jìn)行以下研究：

1. 干細(xì)胞自我更新（Stem cell self-renewal）[1,2]
2. 血統(tǒng)規(guī)格（Lineage specification）[3]
3. 癌細(xì)胞表性（Cancer cell phenotype）[4,5,6]
4. 纖維化（Fibrosis）[7,8]
5. 肝細(xì)胞功能（Hepatocyte function）[9,10,11]
6. 機(jī)械敏感性（Mechanosensing）[12,13,14]

引人注目的是，細(xì)胞是能夠感知環(huán)境柔軟度的改變并有所響應(yīng)，您可以索要獲獎(jiǎng)微電影鏈接。

Soft substrates for stem cells

改變干細(xì)胞培養(yǎng)環(huán)境的柔軟度（matrix stiffness），可以控制干細(xì)胞命運(yùn)。提供給干細(xì)胞舒適的柔軟度，如下：

促進(jìn)自我更新：取自小鼠的肌肉干細(xì)胞，給其提供zui舒適的柔軟環(huán)境（E=12kPa），如同在體內(nèi)，有自我更新修復(fù)的能力[1]；
維持多能性：在E=0.6kPa的基質(zhì)上培養(yǎng)小鼠胚胎干細(xì)胞，在不添加外源性LIF因子的情況下，仍能形成同源性未分化克隆[2]；
Direct lineage specification：成年人間充質(zhì)干細(xì)胞培養(yǎng)在不同彈性（柔軟度）的基質(zhì)上培養(yǎng)，如E=1，E=11和E43時(shí)，分別會(huì)直接向神經(jīng)性，肌源性和成骨性分化[3]。

想了解更多信息，請(qǐng)點(diǎn)擊Matrigen彈性的細(xì)胞培養(yǎng)器皿產(chǎn)品綜合介紹

文獻(xiàn)如下：

1. Gilbert, P.M. et al. 1Substrate elasticity regulates skeletal muscle stem cell self-renewal in culture. Science 329, 1078-1081 (2010).
2. Chowdhury, F. et al. Soft substrates promote homogeneous self-renewal of embryonic stem cells via downregulating cell-matrix tractions. PLoS ONE 5, e15655 (2010).
3. Engler, A.J., Sen, S., Sweeney, H.L. & Discher, D.E. Matrix elasticity directs stem cell lineage specification. Cell 126, 677-689 (2006).
4. Paszek, M.J. et al. Tensional homeostasis and the malignant phenotype. Cancer Cell 8, 241-254 (2005).
5. Levental, K.R. et al. Matrix crosslinking forces tumor progression by enhancing integrin signaling. Cell 139, 891-906 (2009).
6. Tilghman, R.W. et al. Matrix rigidity regulates cancer cell growth and cellular phenotype. PLoS ONE 5, e12905 (2010).
7. Liu, F. et al. Feedback amplification of fibrosis through matrix stiffening and COX-2 suppression. J. Cell Biol 190, 693-706 (2010).
8. Wipff, P.-J., Rifkin, D.B., Meister, J.-J. & Hinz, B. Myofibroblast contraction activates latent TGF-beta1 from the extracellular matrix. J. Cell Biol 179, 1311-1323 (2007).
9. Georges, P.C. et al. Increased stiffness of the rat liver precedes matrix deposition: implications for fibrosis. Am. J. Physiol. Gastrointest. Liver Physiol 293, G1147-1154 (2007).
10.Li, L. et al. Functional modulation of ES-derived hepatocyte lineage cells via substrate compliance alteration. Ann Biomed Eng 36, 865-876 (2008).
11.Semler, E.J., Lancin, P.A., Dasgupta, A. & Moghe, P.V. Engineering hepatocellular morphogenesis and function via ligand-presenting hydrogels with graded mechanical compliance. Biotechnol. Bioeng 89, 296-307 (2005).
12.Friedland, J.C., Lee, M.H. & Boettiger, D. Mechanically Activated Integrin Switch Controls α5β1 Function. Science 323, 642 -644 (2009).
13.Chan, C.E. & Odde, D.J. Traction dynamics of filopodia on compliant substrates. Science 322, 1687-1691 (2008).
14.Dupont, S. et al. Role of YAP/TAZ in mechanotransduction. Nature 474, 179-183 (2011).