C-Jun is essential for the normal activation of the SC repair programme and contributes to SC proliferation and migration [18C20]

C-Jun is essential for the normal activation of the SC repair programme and contributes to SC proliferation and migration [18C20]. this study we investigate the function of Cyr61 in SCs. Results We observed Cyr61 was expressed both in vivo and in vitroThe promoting effect of Cyr61 on SC proliferation and migration was through autocrine and paracrine mechanisms. SCs expressed v3 integrin and the effect of Cyr61 on SC proliferation and migration could be blocked via v3 integrin. Cyr61 could influence c-Jun protein expression in cultured SCs. Conclusions In this study, we found that Cyr61 promotes SC proliferation and migration via v3 integrin and regulates c-Jun expression. Our study contributes to the understanding of cellular and molecular mechanisms underlying SCs function during nerve injury, and thus, may facilitate the regeneration of peripheral nerves after injury. Supplementary Information The online N6-Cyclohexyladenosine version contains supplementary material available at 10.1186/s12860-021-00360-y. strong class=”kwd-title” Keywords: Schwann N6-Cyclohexyladenosine cells, Cyr61, Proliferation, Migration Background Peripheral nerve injury is usually a common clinical problem. It seriously affects the quality of life in patients and results in interpersonal and economic burdens. The treatment for peripheral nerve injury includes nerve suturing, autogenous nerve transplantation, and tissue-engineered nerve transplantation. These treatments promote the functional recovery of hurt nerves [1]. However, to date, the clinical effects of these therapies have not been CD47 acceptable. Understanding the cellular and molecular mechanisms of peripheral nerve injury will be helpful for the clinical treatment of peripheral nerve injury. Compared to peripheral nerve injury in the central nervous system (CNS), SCs are the main glial cells in peripheral nerves and have a robust ability to regenerate [2]. Following peripheral nerve injury, SCs start to proliferate and migrate to the hurt site to obvious axon and myelin debris and build bands of Bngner [3]. In addition, SCs secrete a large number of neurotrophic factors to support the survival of neurons and produce a conducive microenvironment for nerve regeneration [4]. These events rely on the amazing ability of SCs to transform into a potent repair phenotype. SCs de-differentiate into a proliferative, immature-like state via the activation of the JUN dependent repair program [5]. After peripheral nerve injury, axon breaks, and SCs drop contact with their axons. SCs can survive in the absence of axons which is usually important for subsequent nerve regeneration. This is in part because of the ability of SCs to support their survival through autocrine mechanisms [6]. Factors that accelerate SCs proliferation during the early stages after peripheral nerve injury and/or promote SCs migration and myelination during the later stages after nerve injury benefit nerve regeneration and functional recovery [3]. However, the precise mechanisms for this are unclear. Considering the crucial role played by SCs, identifying factors that can accelerate the proliferation and migration of SCs may help promote the repair and regeneration of peripheral nerves after injury. Cysteine-rich protein 61 (Cyr61, also known as CCN1) is usually a member of the CCN family of matrix cell proteins. Cyr61 is usually a secretory protein of the CCN family signal protein related to ECM [7]. It can regulate a wide range N6-Cyclohexyladenosine of cell activities, including cell adhesion, migration, proliferation, differentiation, apoptosis, and aging by interacting with integrin receptors around the cell surface [8]. Previous studies have exhibited that Cyr61 stimulates the migration of easy muscle mass cells [9], fibroblasts [10], endothelial cells [11], and some malignancy cells [12C14]. Cyr61 has also been observed in the nervous system. For example, Cyr61, as a dendrite growth regulator of hippocampal neurons, controls dendrite growth in an 1 integrin-dependent manner [15]. Cyr61 also plays a role in tissue repair. N6-Cyclohexyladenosine During the process of skin wound healing, N6-Cyclohexyladenosine Cyr61 can accelerate re-epithelialization by promoting the migration and proliferation of keratinocytes [16]. A recent study found that SCs transformed into repair mediating SCs after FYT702P treatment and the secretion levels of Cyr61 in SC conditioned medium increased. This indicated.

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