Abstract
An effective regulation of quiescence plays a key role in the differentiation, plasticity, and prevention of stem cells from becoming malignant. The state of quiescence is being controlled by the pRb family proteins which show overlapping functions in cell cycle regulation; however, their roles in controlling the proliferation of mesenchymal stem cells (MSCs) remain to be understood. This study investigated the regulation of transient quiescence using growth curves, proliferation assay, the cytometric evaluation of cell cycle, Western blotting, and the electromobility gel shift assay (EMSA) on synchronized MSCs of the C3H10Т1/2 and control cells with different statuses of pRb proteins. It has been found that functional steady-state level of p130 but not pRb plays a critical role for entering, exiting, and maintenance of transient quiescence in multipotent mesenchymal stem cells.
Highlights
PRb, p130, and p107 comprising the pocket protein family are considered ubiquitous cell cycle regulators with overlapping functions [1]
The results suggest that the entering and maintenance of the quiescent state in mesenchymal stem cells (MSCs) is associated with the functional steadystate level of p130 but not The retinoblastoma susceptibility gene product embryonic stem cells (ESCs) (pRb)
It is believed that commitment to differentiation occurs at the early G1 phase that lasts until the G1 restriction point and is under the control of pRb proteins [1, 25]
Summary
PRb, p130, and p107 comprising the pocket protein family are considered ubiquitous cell cycle regulators with overlapping functions [1]. All three pocket proteins are required to be inactivated for the loss of cell cycle control, ability to differentiate, and induction of cell immortality [2]. These observations support the idea of the functional redundancy of pocket proteins whose physiological relevance is currently not completely clear [3]. PRb deficiency targets genes that encode cell cycle regulatory proteins, the expression of which is regulated by E2f1-3 [5, 6]. The loss of p107/p130 alters the expression of genes regulating quiescence in response to growth or differentiation signals [6]
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