Department of Internal Medicine, University of Missouri School of Medicine, Columbia, MO, USA.
Oxid Med Cell Longev. 2010 Sep-Oct;3(5):290-303. doi: 10.4161/oxim.3.5.13653. Epub 2010 Sep 1.
The pericyte's role has been extensively studied in retinal tissues of diabetic retinopathy; however, little is known regarding its role in such tissues as the pancreas and skeletal muscle. This supportive microvascular mural cell, plays an important and novel role in cellular and extracellular matrix remodeling in the pancreas and skeletal muscle of young rodent models representing the metabolic syndrome and type 2 diabetes mellitus (T2DM). Transmission electron microscopy can be used to evaluate these tissues from young rodent models of insulin resistance and T2DM, including the transgenic Ren2 rat, db/db obese insulin resistant - T2DM mouse, and human islet amyloid polypeptide (HIP) rat model of T2DM. With this method, the earliest pancreatic remodeling change was widening of the islet exocrine interface and pericyte hypercellularity, followed by pericyte differentiation into islet and pancreatic stellate cells with early fibrosis involving the islet exocrine interface and interlobular interstitium. In skeletal muscle there was a unique endothelial capillary connectivity via elongated longitudinal pericyte processes in addition to pericyte to pericyte and pericyte to myocyte cell-cell connections allowing for paracrine communication. Initial pericyte activation due to moderate oxidative stress signaling may be followed by hyperplasia, migration, and differentiation into adult mesenchymal cells. Continued robust oxidative stress may induce pericyte apoptosis and impaired cellular longevity. Circulating antipericyte autoantibodies have recently been characterized, and may provide a screening method to detect those patients who are developing pericyte loss and are at greater risk for the development of complications of T2DM due to pericytopathy and rarefaction. Once detected, these patients may be offered more aggressive treatment strategies such as early pharmacotherapy in addition to life style changes targeted to maintaining pericyte integrity. In conclusion, we have provided a review of current knowledge regarding the pericyte and novel ultrastructural findings regarding its role in metabolic syndrome and T2DM.
周细胞的作用在糖尿病视网膜病变的视网膜组织中得到了广泛的研究；然而，对于其在胰腺和骨骼肌等组织中的作用知之甚少。这种支持性的微血管壁细胞在年轻啮齿动物模型的胰腺和骨骼肌中的细胞和细胞外基质重塑中发挥着重要的、新颖的作用，这些模型代表了代谢综合征和 2 型糖尿病（T2DM）。透射电子显微镜可用于评估来自胰岛素抵抗和 T2DM 年轻啮齿动物模型的这些组织，包括转基因 Ren2 大鼠、db/db 肥胖胰岛素抵抗-T2DM 小鼠和 T2DM 的人类胰岛淀粉样多肽（HIP）大鼠模型。通过这种方法，最早的胰腺重塑变化是胰岛外分泌界面变宽和周细胞细胞增多，随后周细胞分化为胰岛和胰腺星状细胞，早期纤维化涉及胰岛外分泌界面和小叶间间质。在骨骼肌中，除了周细胞与周细胞和周细胞与肌细胞的细胞间连接外，还有独特的内皮毛细血管连接，通过伸长的纵向周细胞过程，允许旁分泌通讯。由于中度氧化应激信号，最初的周细胞激活可能随后是增生、迁移和分化为成体间充质细胞。持续的强烈氧化应激可能诱导周细胞凋亡和细胞寿命受损。最近已经描述了循环抗周细胞自身抗体，并且可能提供一种筛选方法来检测那些正在失去周细胞并且由于周细胞病和稀疏而处于发展为 T2DM 并发症的更高风险的患者。一旦检测到，这些患者可能会接受更积极的治疗策略，例如除了生活方式改变外，还进行早期药物治疗，以维持周细胞的完整性。总之，我们提供了关于周细胞的当前知识的综述，以及关于其在代谢综合征和 T2DM 中的作用的新的超微结构发现。
