壁细胞（周细胞和平滑肌细胞）是血管系统的组成部分，存在于脑、肺、肾、脾等多种器官的血管系统中。大量研究集中于壁细胞在特定器官或某些疾病中的作用。然而，壁细胞于生理状况下不同器官中的形态、位置、分布是否相同尚无报道。胶质瘤是常见的致命脑肿瘤，一个重要特征是存在为肿瘤生长与增殖提供适宜环境与营养的丰富血管，而壁细胞是包裹血管内皮的支持细胞，其在胶质瘤中发挥的作用尚不清楚。揭示不同器官中壁细胞的生理参数和在胶质瘤增殖中的形态变化与作用将有助于进一步研究其在生理状态和病理（胶质瘤）条件下的作用，加深对壁细胞的了解，为今后的研究提供有价值的参考。我们通过基因鉴定证实PDGFRβ-tdTomato基因工程小鼠成功繁育。对比野生型C57BL/6J小鼠，基因工程小鼠的形态外观和繁殖等无差异，组织HE切片分析显示脏器发育无异常。Tamoxifen诱导下基因工程小鼠的Cre重组酶活性至第7天充分表达。基于此，通过三维共聚焦免疫荧光成像与流式细胞术，使用PDGFRβ-tdTomato转基因小鼠特异性地表征不同器官中壁细胞的比例、密度、血管覆盖率和平均大小等参数。结果表明，壁细胞在心脏的比例最高（24.5%），在脾和脑的白髓中比例最低（9.5%）。壁细胞密度在肾髓质最高（46060个/mm³），肝脏最低（12619个/mm³）。脑部壁细胞覆盖率最高（90.2%），脾白髓最低（8.5%）。在荧光可视化壁细胞的基因工程小鼠上分别利用异硫氰酸荧光素-葡聚糖标记血管和青色荧光标记肿瘤细胞，使用玻璃圆片与固定环替代小鼠颅骨，实现了活体状态下长期稳定地动态跟踪小鼠接种脑肿瘤后血管及血管支持细胞的形态结构变化。连续靶向敲除壁细胞后，早期可以短暂抑制胶质瘤增殖，中晚期则促进胶质瘤增殖。研究结果证实仅在早期抑制壁细胞可以阻遏胶质瘤增殖。胶质瘤进展前敲除壁细胞则促进胶质瘤增殖，突显了壁细胞抑制胶质瘤增殖中的保护性作用。接种GL261-CFP后观察到胶质瘤增殖侵袭的动态过程及肿瘤内血管形态结构呈现异质性、迂曲、分枝不齐，游离壁细胞的比例增多。胶质瘤中壁细胞形态发生显著变化，通过Myh11-CreER^T2(+/-):Rosa26-tdTomato(+/-):CX₃CR1-GFP(+/-)小鼠在活体上证实胶质瘤增殖过程中存在Myh11+壁细胞表达小胶质细胞的CX₃CR1+标志物，免疫荧光证实胶质瘤中PDGFRβ+壁细胞与IBA1+小胶质细胞存在共定位，证明壁细胞获得了小胶质细胞的表型。

Mural cells (pericytes and smooth muscle cells) are components of the vascular system, which exist in the vascular system of brain, lung, kidney, spleen and other organs. Numerous studies focused on the role of mural cells in specific organs or certain diseases. However, whether the morphology, location and distribution of mural cells are the same in different organs under physiological conditions, and the role of mural cells in glioma is still unclear. Glioblastoma (GBM) is the most common and universally lethal brain tumor. The presence of abundant vasculature is a defining feature of GBM, providing crucial environmental signals that facilitate tumor growth and advancement. Mural cells, which envelop the endothelial lining of blood vessels, play a vital role in the formation of GBM vasculature. Revealing the physiological parameters of mural cells in different organs and their morphological changes and functions in glioma proliferation will greatly contribute to the further study of their role in physiological and pathological conditions, deepen our understanding of the morphology of mural cells, and provide a valuable reference for future research. We confirmed that PDGFRβ-Cre(+/-):Rosa26-tdTomato (+/-) genetically engineered mice were successfully bred by genetic identification. In comparison to C57BL/6J mice, genetically engineered mice exhibited no discernible differences in morphology, appearance, or reproductive capabilities. Histological examination of tissue sections revealed normal organ development. Cre recombinase activity in genetically engineered mice, induced by Tamoxifen, was fully activated by the 7th day. Subsequently, three-dimensional confocal immunofluorescence imaging and flow cytometry techniques were employed to assess the proportion, density, vascular coverage, and average size of mural cells in various organs using PDGFRβ-tdTomato transgenic mice.The results showed that the proportion of mural cells was the highest in the heart (24.5%) and the lowest in the white pulp of the spleen and brain (9.5%). The mural cell density was the highest in the renal medulla (46060 / mm³) and the lowest in the liver (12619 / mm³). The cerebrovascular mural cells exhibited the highest coverage rate at 90.2%, while the spleen white pulp showed the lowest coverage rate at 8.5%. Genetically engineered mice with fluorescent visual mural cells were utilized in the study, with fluorescein isothiocyanate-glucan used to label blood vessels and cyan fluorescence to label tumor cells. Additionally, glass discs and fixed rings were employed to replace the skulls of the mice. This methodology allowed for the long-term in vivo tracking of morphological and structural changes in blood vessels and vascular mural cells following brain tumor inoculation. Following the inoculation of GL261-CFP, observations were made regarding the dynamic processes of proliferation and invasion of glioma, alterations in vascular morphology and structure, and an increase in free mural cells within the tumor. Significant changes were noted in the morphology of mural cells in glioma. The transdifferentiation of mural cells into microglia was confirmed in Myh11(+/-):Rosa26-tdTomato(+/-):CX3CR1-GFP(+/-) mice in vivo. Targeted knockout of mural cells demonstrated the ability to inhibit glioma proliferation in the early stages while promoting proliferation in the middle and late stages, as supported by the findings.