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周细胞在子宫内膜异位症血管生成中的作用赵采云;尹利荣;孙俊杰【摘要】Objective To study the expression of pericyte and the association between pericyte and angiogenesis in the endometriosis. Methods the endometriosis group is consisted of 20 ectopic endometrium, 20 eutopic endometrium dur-ing proliferation phase, 20 eutopic endometrium during secretory phase of patient with endometriosis. The control group (non-endometriosis ) include 20 normal endometrium during proliferation phase and 20 normal endometrium during prolifer-ation phase of women without entometriosis. The histological morphology parameters such as mean density of microvessel (MVD), pericytes number(PN)as well as the average ratio of pericyte to endothelial cells in microvessels were measured by immunohistochemical and morphological assesses. Results The expression of MVD was lower in the normal endometrium and eutopic endometrium compared with it in ectopic endometrium tissue. The difference of the MVD among the different groups was statistical significant (P<0.05). The expression of MVD in secretory phase endometrium was higher than it in proliferative phase endometrium(P<0.05), and it shows no significant difference between eutopic endometrium and normal endometrium. The expression of PN andPN/MVD in ectopic and eutopic endometrium in EMs group were lower than those in control group. However, we also found that the difference of PN and PN/MVD was not statistically significant. Conclusion Pericytes playan important role in angiogenesis of the endometriosis ,and pericyte coverage contribute to maturing of func-tional vasculature of endometriosis.%目的：探讨周细胞在子宫内膜异位症（EMs）血管生成中的作用。
血管生成与女性生殖系统疾患关系探讨
王蕾;孙祖越;曹霖
【期刊名称】《生殖与避孕》
【年(卷),期】2007(27)1
【摘要】女性生殖器官如子宫、卵巢等均为血流量较高,且间断性快速生长的组织,血管生成对于这些组织的生长及功能具有非常重要的作用.而目前对新生血管抑制剂的研究报道几乎都集中在肿瘤治疗上,研究表明,子宫内膜异位症、胚泡植入、子宫肌瘤、多囊卵巢综合征等病理生理过程均与血管生成相关.新生血管抑制剂与常规的激素治疗相比,具有很多优点,如疗效好,不良反应小等,在不远的将来也许会成为女性生殖系统疾患的一种新的治疗方法.
【总页数】4页(P52-55)
【作者】王蕾;孙祖越;曹霖
【作者单位】上海市计划生育科学研究所药理毒理学研究室,中国生育调节药物毒理检测中心,上海,200032;上海市计划生育科学研究所药理毒理学研究室,中国生育调节药物毒理检测中心,上海,200032;上海市计划生育科学研究所药理毒理学研究室,中国生育调节药物毒理检测中心,上海,200032
【正文语种】中文
【中图分类】R71
【相关文献】
1.妇炎康冲剂治疗女性生殖系统感染性疾患40例 [J], 艾广萍;朱亚玲;张红梅;陈永峰
2.肠液及血清标本CA-50与大肠疾患的关系探讨 [J], 肖淑兰;蔡霞媚
3.血管生成素2及CD105在急性心肌梗死大鼠中的表达及与梗死面积的关系探讨[J],
4.基于血管生成拟态与肿瘤干细胞的关系探讨中医药干预肿瘤转移的可能机制 [J], 王学谦;林洪生;赵志正;张英
5.幽门螺杆菌感染及其毒力相关基因cagA的分布与临床胃疾患关系探讨 [J], 高艳萍;原素梅;郝素珍
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血管生成相关基因血管生成是指在生物体内形成新的血管，以供应氧气和营养物质。
这个过程对于维持正常生物体的生长和发育至关重要。
血管生成是一个复杂的过程，涉及许多基因的调控和相互作用。
在血管生成过程中，许多基因起到关键作用。
其中，一些基因参与血管内皮细胞的增殖、迁移和分化，调控血管的形成和分支。
另一些基因则参与血管平滑肌细胞的生长和收缩，从而调节血管的功能。
例如，血管内皮生长因子（VEGF）家族是血管生成过程中最为重要的调节因子之一。
VEGF家族成员包括VEGF-A、VEGF-B、VEGF-C和VEGF-D 等。
这些因子通过结合它们的受体，如VEGFR-1和VEGFR-2等，促进血管内皮细胞的增殖和迁移，从而促进新血管的形成。
除了VEGF家族，还有其他一些重要的基因参与血管生成过程。
例如，基本纤维生长因子（bFGF）家族和血小板衍生生长因子（PDGF）家族也起到重要的调节作用。
这些因子通过与它们的受体结合，调控血管内皮细胞和平滑肌细胞的增殖和分化，从而促进血管的形成。
此外，一些转录因子也参与血管生成的调控。
例如，转录因子HIF-1（hypoxia-inducible factor 1）在低氧条件下被激活，促进VEGF的表达，从而刺激血管生成。
另外，转录因子FOXO（forkhead box O）家族也参与血管生成过程的调控，通过调节一系列基因的表达，影响血管内皮细胞的增殖和迁移。
总的来说，血管生成过程涉及许多基因的调控和相互作用。
这些基因通过调节血管内皮细胞和平滑肌细胞的增殖、迁移和分化，参与新血管的形成。
对于进一步理解血管生成的机制和开发相关疾病的治疗方法，深入研究这些血管生成相关基因具有重要意义。
MCPIP1通过调节VEGFA-ERK途径促进胶质瘤细胞的增殖、迁移和血管生成摘要：MCPIP1是一种新型的转录因子，可通过调节多种信号通路影响不同细胞的生长、分化和凋亡等生物学过程。
本研究旨在探讨MCPIP1在胶质瘤细胞增殖、迁移和血管生成中的作用及其机制。
我们发现MCPIP1在人脑胶质瘤组织和细胞系中高表达，过表达MCPIP1可显著促进胶质瘤细胞的增殖和迁移，同时增强VEGFA/ERK信号通路的活性。
进一步实验发现，MCPIP1通过直接与VEGFA基因启动子结合，增强VEGFA的转录和表达，同时通过调节ERK1/2磷酸化水平影响VEGFA信号通路的下游效应，从而促进胶质瘤细胞的血管生成能力。
这些结果表明MCPIP1可能是促进胶质瘤发生和发展的一个新的靶点，有望成为预防和治疗胶质瘤的重要药物靶点。
关键词：胶质瘤，MCPIP1，VEGFA，ERK，血管生成。
Abstract: MCPIP1 is a novel transcription factor that can affect various biological processes such as growth, differentiation, and apoptosis in different cells by regulating multiple signaling pathways. This studyaims to investigate the role and mechanism of MCPIP1in glioma cell proliferation, migration, and angiogenesis. We found that MCPIP1 was highly expressed in human glioma tissues and cell lines. Overexpression of MCPIP1 significantly promoted gliomacell proliferation and migration, while enhancing the activity of the VEGFA/ERK signaling pathway. Further experiments revealed that MCPIP1 directly bound to the VEGFA gene promoter, increased VEGFA transcription and expression, and affected the downstream effects of the VEGFA signaling pathway by regulating the phosphorylation levels of ERK1/2, thereby promotingthe angiogenic ability of glioma cells. These results suggest that MCPIP1 may be a novel target forpromoting glioma occurrence and development, and may become an important drug target for prevention and treatment of glioma.Keywords: Glioma, MCPIP1, VEGFA, ERK, angiogenesisGlioma is a highly invasive and aggressive tumor that remains one of the most challenging diseases to treat. Therefore, there is an urgent need to identify new molecules and pathways that can be targeted to inhibit glioma growth and progression. In recent years, research has focused on the role of MCPIP1 in cancer, including its involvement in angiogenesis, which is a critical process for tumor development and progression.The study found that MCPIP1 promoted angiogenesis in glioma by upregulating the expression of VEGFA. The VEGFA gene is a key regulator of angiogenesis thatpromotes the growth of new blood vessels. Increased VEGFA expression is often observed in various types of tumors and is associated with poor prognosis.The study also revealed that MCPIP1 regulates the downstream effects of the VEGFA signaling pathway by regulating the phosphorylation levels of ERK1/2.ERK1/2 is an important signaling molecule that regulates many cellular processes, including cell proliferation, differentiation, and survival. In glioma, dysregulation of ERK1/2 signaling has been implicated in tumor growth and progression.Overall, these findings suggest that MCPIP1 may be a promising target for anti-angiogenic therapy in glioma. Targeting MCPIP1 could inhibit VEGFA expression and downstream signaling, thus suppressing angiogenesisand inhibiting tumor growth. Further studies are needed to explore the potential of MCPIP1 as a therapeutic target for gliomaIn addition to targeting MCPIP1, other approaches have been explored for anti-angiogenic therapy in glioma. One such approach is inhibition of vascularendothelial growth factor receptor 2 (VEGFR2), whichis the primary receptor for VEGFA. Inhibition of VEGFR2 reduces VEGFA-mediated angiogenesis and hasbeen shown to slow tumor growth in preclinical models of glioma. Clinical trials of VEGFR2 inhibitors, such as bevacizumab, have shown promise in treating recurrent glioblastoma, although there are concerns about resistance to this therapy and its effects on normal brain tissue.Another approach to anti-angiogenic therapy in glioma is targeting the perivascular niche, which is the microenvironment surrounding blood vessels in tumors. The perivascular niche is important for supporting tumor growth and angiogenesis, and has been shown to be associated with therapy resistance and tumor recurrence. Targeting the perivascular niche, either through direct targeting of perivascular cells or via inhibition of signaling pathways that regulate niche formation and maintenance, may be effective in inhibiting tumor growth and improving treatment outcomes.Additionally, some studies have investigated anti-angiogenic therapy in combination with other treatments, such as chemotherapy or immunotherapy. Preclinical studies have shown that combining anti-angiogenic therapy with chemotherapy can enhance tumor response and reduce resistance to chemotherapy. Clinical trials of this approach in glioblastoma haveyielded mixed results, but further investigation is ongoing. Combining anti-angiogenic therapy with immunotherapy, such as immune checkpoint inhibitors,is also being explored as a potential strategy to improve treatment outcomes in glioma.In conclusion, targeting angiogenesis is a promising approach to treating glioma, a highly vascularized and aggressive brain tumor. MCPIP1 is a novel target for anti-angiogenic therapy, and its inhibition may be effective in suppressing angiogenesis and inhibiting tumor growth. However, further studies are needed to fully understand the mechanisms of MCPIP1 in glioma and to explore its potential as a therapeutic target. Other approaches to anti-angiogenic therapy in glioma, including targeting VEGFR2, the perivascular niche, and combination with other treatments, are also being explored and may yield promising resultsIn addition to targeting MCPIP1, there are other promising approaches to anti-angiogenic therapy in glioma that are currently being explored. One such approach involves targeting VEGFR2, a receptor for vascular endothelial growth factor that plays acritical role in tumor angiogenesis. Bevacizumab, a monoclonal antibody that targets VEGF, has been approved for the treatment of recurrent glioblastomaand has shown promise in clinical trials. However, its effectiveness is limited by the development of resistance and the lack of overall survival benefit.Another approach to anti-angiogenic therapy in glioma is to target the perivascular niche, which is a microenvironment around blood vessels that supports tumor growth and development. The perivascular nicheis enriched with stem cells, immune cells, and extracellular matrix components that facilitate tumor cell survival and proliferation. Targeting the perivascular niche may disrupt the tumor microenvironment and improve the efficacy of anti-angiogenic therapy in glioma.Combination therapy is another strategy for enhancing the effectiveness of anti-angiogenic therapy in glioma. For instance, combining anti-angiogenic therapy with immunotherapy may enhance the antitumor immune response and produce a synergistic effect. Preclinical studies have shown that combining bevacizumab with immune checkpoint inhibitors or adoptive T celltherapy can improve survival and reduce tumor growthin glioma models. Similarly, combining anti-angiogenic therapy with chemotherapy or radiation therapy may enhance their cytotoxic effects and improve treatment outcomes.In summary, anti-angiogenic therapy has emerged as a promising strategy for the treatment of glioma, and the identification of novel targets such as MCPIP1 may further improve its efficacy. However, further research is needed to fully understand the mechanisms of tumor angiogenesis and to develop more effective and specific anti-angiogenic agents. Combination therapy and targeted approaches to the perivascular niche are also promising strategies for improving the efficacy of anti-angiogenic therapy in gliomaIn conclusion, anti-angiogenic therapy holds great potential for the treatment of glioma. MCPIP1 is a potential novel target that can improve the efficacy of this therapy. However, more research is necessary to understand tumor angiogenesis mechanisms and develop effective and specific anti-angiogenic agents. Combination therapy and targeted approaches to the perivascular niche are also promising strategies for improving the efficacy of anti-angiogenic therapy。
Mir-30的研究进展易韬【摘要】微小RNA(miRNA)是内源性的非编码小RNA,对基因表达进行转录后调控,是近年来分子医学领域最重要的发现之一.目前已发现上千种miRNA,虽然已经有大量针对miRNA的研究,但是绝大部分miRNA的生物学功能仍然有待研究.已查明miR-30的家族成员与多种生理过程相关,有可能成为疾病的新的治疗靶点.本文就miR-30的基本特征及作用作一综述.【期刊名称】《四川解剖学杂志》【年(卷),期】2013(021)004【总页数】5页(P24-27,60)【关键词】MicroRNA;miR-30;靶基因【作者】易韬【作者单位】四川大学华西第二医院妇科肿瘤生物治疗实验室,成都610041【正文语种】中文【中图分类】R737MicroRNAs 家族是一类内源性的非编码小RNA 分子，大多数miRNA 来自于70～90个碱基大小的单链RNA 前体，经过Dicer酶加工后产生成熟的19～25个小核苷酸［1－4］，在基因表达的转录后调节中发挥重要作用，参与多种细胞过程，包括信号转导、器官发育、疾病发生、药理和毒理作用等［5］。
miRNAs拥有复杂的调节网络，一个miRNA 可以调控多个基因的表达，而多个miRNAs 也可以组合来调控某个基因的表达。
虽然已经有大量针对miRNA 的研究，但是绝大部分miRNA 的生物学功能仍然有待研究。
miR－30家族是由6个位于人类1，6，和8染色体上的基因编码，包括5 个成员，miR－30a、miR－30b、miR－30c、miR－30d、miR－30e，它们之间的序列同源性非常高。
microRNA 5’端2－8个核苷酸被称为种子序列（seed sequence），是靶标结合最关键的位点［6］。
种子序列与mRNA 转录目标之间的互补性和mRNA 位点的二级结构是靶向识别的关键因素［7－8］。
由于miR－30家族的microRNA 的核苷酸种子序列有较高的保守性和重叠的表达模式，提示miR－30家族在生物功能上可能发挥关键作用（图1）［9］。
微血管密度和血管生成拟态在子宫腺肌症中的表达及意义王木森;孙春风;柳雅玲【摘要】Objective:To investigate the microvascular density and angiogenesis mimicry in the expression and signifi-cance of uterine adenomyosis. Methods:Forty patients with histopathologic diagnosis of uterine adenomyosis were selected as observation group in our hospital between 2012 and October 10,2014,then 40 cases of adenomyosis uterine hysterectomy patients were selected as control group. Using immunohistochemical S-P method,CD31 monoclonal antibody expression of two groups of patients were analyzed. Special staining PAS was used to observe angiogenesis mimicry in both groups. Results:In the uterine adenomyosis ectopic endometrium and the lining in the endometrium in the observation group,and endometrial tissue in the control group in the organization,CD31 markers of microvascular density were 32. 850,22. 275 and 14. 275,respectively. The mean between the two in the q test showed that the comparison between the two groups was statistically significant(P < 0. 001). Angiogenesis mimicry was not observed in the three groups by PAS staining. Conclusion:In the uterine adenomyosis,ectopic endometrium,the lining in ectopic and microvascular density of the control reduced in turn. Angiogenic factors and ectopic endometrial invasive ability have a close relationship,which may be one of the important factors promoting ectopic endometrium invasion of uterine glands.%目的：探讨微血管密度和血管生成拟态在子宫腺肌症中的表达及意义。
CDK6导致肿瘤的机制研究进展董一楠;张新伟;魏枫【摘要】细胞周期的异常调控导致细胞过度增殖是人类肿瘤发生的重要原因之一,目前已发现CDK6和CDK4是细胞周期的重要调控因子,促进细胞周期正向进行,且在人类大多数肿瘤中过度激活,与肿瘤的发生密切相关.最近,研究证实以CDK4/6为靶点的肿瘤治疗有广泛前景.但是对于CDK6过度激活导致肿瘤发生的机制尚不完全清楚.因此有必要进一步了解CDK4/6在细胞周期调控通路、细胞分化中的作用及其在不同类型肿瘤中的异常表达,对深入了解肿瘤的发生机制及治疗有重大意义.本文拟对CDK6的结构、生物学功能、促进肿瘤的相关机制,以及其抑制剂的临床应用等方面的内容进行阐述.%Cell-cycle deregulation leading to excessive cell proliferation is an important mechanism of human tumorigenesis. CDK6 and CDK4 have been found to be significant regulators of cell cycle, particularly in promoting cell -cycle progress. Moreover, these proteins are usually overly active in most tumors and closely related to tumor development. Recently, research has confirmed CDK4/6 as prospective targets for cancer therapy. However, the mechanism of excessive CDK6 activation leading to tumorigenesis is not completely understood. Therefore, further understanding of the role of CDK4/6 in cell -cycle regulatory pathways and cell differenti-ation is essential, as well as their overexpression in different types of tumors. This information will elucidate the mechanisms of tumor development and treatment. Therefore, this review intends to discuss the structure and biological function of CDK6,the role and mecha-nism of CDK6 in carcinogenesis, and the clinical application of CDK6 inhibitors.【期刊名称】《中国肿瘤临床》【年(卷),期】2015(042)019【总页数】5页(P973-977)【关键词】CDK6;肿瘤;细胞周期;细胞分化;抑制剂【作者】董一楠;张新伟;魏枫【作者单位】天津医科大学肿瘤医院肿瘤研究所免疫研究室,国家肿瘤临床医学研究中心,天津市肿瘤免疫与生物治疗重点实验室天津市300060;天津医科大学肿瘤医院肿瘤研究所免疫研究室,国家肿瘤临床医学研究中心,天津市肿瘤免疫与生物治疗重点实验室天津市300060;天津医科大学肿瘤医院肿瘤研究所免疫研究室,国家肿瘤临床医学研究中心,天津市肿瘤免疫与生物治疗重点实验室天津市300060【正文语种】中文细胞周期的异常调控是人类肿瘤发生的主要原因之一［1］。
血管生成的分子生物学调控机制研究血管生成是一个复杂的过程，涉及到许多分子生物学调控机制。
在治疗心脑血管疾病和癌症方面，对血管生成机制的深入研究具有重要的意义。
下面，本文将从血管生成的定义、分子机制的发现等方面进行探讨。
血管生成的定义血管生成是指在生物体内形成新血管的过程，是组织生长和再生的基础。
血管生成主要通过两种方式进行：一种是形成新的血管，另一种是重建 arteriolar 和capillary 网络。
这两种过程包括内皮细胞分裂、血管生成素的作用、基质分解蛋白酶的分泌以及血管平滑肌细胞增殖等。
基本发现关于血管生成的基本发现，最早可以追溯到上世纪五六十年代。
当时，科学家们发现，肿瘤的生长需要血管的供应。
在二十世纪末，分子生物学技术的发展为血管生成研究提供了全新的手段。
以下是与血管生成相关的分子机制的一些发现。
VEGFVEGF 是血管生成的主要诱导因子，它可以促进内皮细胞的分裂和血管的增殖，并且参与基质分解和肿瘤血管的重建。
VEGF 在肿瘤血管生成中起着关键作用。
VEGF 的表达和生物学功能受到多种信号通路的调控。
例如，雌激素会促进VEGF 的表达。
VEGF 在选择性地下调调节细胞因子生长因子 1 的表达和活性中也发挥了重要作用。
抗癌药物 Sunitinib 可以通过阻断 VEGF 的信号通路来抑制肿瘤的生长。
Sunitinib 对一些肿瘤具有良好的疗效，因此成为了近年来研究的重点。
mTOR 信号通路mTOR 信号通路是当前研究的热点之一。
mTOR 信号通路是一个与细胞增殖和代谢有关的复杂机制。
在血管形成中，mTOR 可以通过促进蛋白质合成和细胞分裂来增强血管生成，因此成为了治疗肿瘤的目标。
PDGFPDGF 对血管生成也有重要作用。
它可以促进肌管的增殖和造血干细胞的扩增，从而促进血管的形成和修复。
PDGF 在心脑血管疾病中的逆转和修复过程中发挥了作用。
microRNAmicroRNA 也可以调控血管生成，通过调节血管生成素和其它信号分子的表达来影响血管芽的形成和内皮细胞的增殖。
