ECM Degradation and Macrophage Polarization in Endogenous Stem Cell Recruitment

内源干细胞招募中的 ECM 降解和巨噬细胞极化

基本信息

  • 批准号:
    8122283
  • 负责人:
  • 金额:
    $ 4.68万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2010
  • 资助国家:
    美国
  • 起止时间:
    2010-07-06 至 2014-07-05
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): Regeneration in response to injury is limited to select tissues in adult mammals. The default response to injury in most other tissues involves the processes of inflammation and scar tissue formation (i.e., repair). The microenvironment of the wound plays an important role in determining regeneration versus scar in adult mammals. In species capable of regenerating complex tissues, stem cells recruited to the wound microenvironment promote a process known as epimorphic regeneration. Biologic scaffolds composed of porcine derived extracellular matrix (ECM) have successfully been used in over one million human patients to create a wound microenvironment that promotes site-specific, non-inflammatory repair of a variety of soft tissues. Implantation of an ECM scaffold following tissue injury results in rapid degradation, release of bioactive peptides, local macrophage polarization, and endogenous stem cell recruitment. The mechanisms underlying ECM mediated stem cell recruitment in vivo are well not understood, but may partially be mediated by molecules released following ECM degradation. Polarized macrophages are also capable of recruiting stem cells in vitro, but their contribution to endogenous stem cell recruitment in vivo is not well understood. The overall goal of the present study is to investigate: (1) role of ECM degradation in stem cell recruitment in vitro and in vivo, (2) the role of ECM degradation on macrophage polarization in vitro and in vivo, and (3) the relative contributions of ECM degradation and polarized macrophages upon endogenous stem cell recruitment in vivo. The findings of the present study further inform us on the on the role of the innate immune system in promoting tissue regeneration, and it will serve as the foundation of future studies to further investigate the mechanisms underlying interaction between extracellular matrix components, the innate immune system, and endogenous stem cells.
描述(由申请人提供):损伤后的再生仅限于成年哺乳动物的选定组织。大多数其他组织对损伤的默认反应涉及炎症和瘢痕组织形成的过程(即,修复)。伤口的微环境在成年哺乳动物中决定再生与瘢痕的关系中起着重要作用。在能够再生复杂组织的物种中,招募到伤口微环境中的干细胞促进了一种称为表型再生的过程。由猪源性细胞外基质(ECM)组成的生物支架已成功用于超过一百万例人类患者,以创建伤口微环境,促进各种软组织的位点特异性非炎症修复。在组织损伤后植入ECM支架导致快速降解、生物活性肽的释放、局部巨噬细胞极化和内源性干细胞募集。ECM介导的干细胞体内募集的机制尚不清楚,但可能部分由ECM降解后释放的分子介导。极化的巨噬细胞也能够在体外募集干细胞,但它们对体内内源性干细胞募集的贡献还不清楚。本研究的总体目标是研究:(1)ECM降解在体外和体内干细胞募集中的作用,(2)ECM降解在体外和体内巨噬细胞极化中的作用,以及(3)ECM降解和极化巨噬细胞在体内内源性干细胞募集中的相对贡献。本研究的结果进一步为我们提供了先天免疫系统在促进组织再生中的作用,并将为进一步研究细胞外基质成分,先天免疫系统和内源性干细胞之间相互作用的机制奠定基础。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

数据更新时间:{{ journalArticles.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ monograph.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ sciAawards.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ conferencePapers.updateTime }}

{{ item.title }}
  • 作者:
    {{ item.author }}

数据更新时间:{{ patent.updateTime }}

Vineet Agrawal其他文献

Vineet Agrawal的其他文献

{{ item.title }}
{{ item.translation_title }}
  • DOI:
    {{ item.doi }}
  • 发表时间:
    {{ item.publish_year }}
  • 期刊:
  • 影响因子:
    {{ item.factor }}
  • 作者:
    {{ item.authors }}
  • 通讯作者:
    {{ item.author }}

{{ truncateString('Vineet Agrawal', 18)}}的其他基金

A Pathogenic Role for the Natriuretic Peptide Clearance Receptor in Heart Failure with Preserved Ejection Fraction.
钠尿肽清除受体在射血分数保留的心力衰竭中的致病作用。
  • 批准号:
    10589324
  • 财政年份:
    2023
  • 资助金额:
    $ 4.68万
  • 项目类别:
A Pathogenic Role for Natriuretic Peptide Receptor-C in Pulmonary Hypertension and Heart Failure with Preserved Ejection Fraction
钠尿肽受体-C 在肺动脉高压和射血分数保留的心力衰竭中的致病作用
  • 批准号:
    10463813
  • 财政年份:
    2021
  • 资助金额:
    $ 4.68万
  • 项目类别:
A Pathogenic Role for Natriuretic Peptide Receptor-C in Pulmonary Hypertension and Heart Failure with Preserved Ejection Fraction
钠尿肽受体-C 在肺动脉高压和射血分数保留的心力衰竭中的致病作用
  • 批准号:
    10301687
  • 财政年份:
    2021
  • 资助金额:
    $ 4.68万
  • 项目类别:
ECM Degradation and Macrophage Polarization in Endogenous Stem Cell Recruitment
内源干细胞招募中的 ECM 降解和巨噬细胞极化
  • 批准号:
    7912172
  • 财政年份:
    2010
  • 资助金额:
    $ 4.68万
  • 项目类别:
ECM Degradation and Macrophage Polarization in Endogenous Stem Cell Recruitment
内源干细胞招募中的 ECM 降解和巨噬细胞极化
  • 批准号:
    8296675
  • 财政年份:
    2010
  • 资助金额:
    $ 4.68万
  • 项目类别:

相似海外基金

Development of small molecule inhibitors as anti-inflammatory agents and antidotes for arsenicals
开发作为抗炎剂和砷解毒剂的小分子抑制剂
  • 批准号:
    10727507
  • 财政年份:
    2023
  • 资助金额:
    $ 4.68万
  • 项目类别:
Discovery of New Anti-Inflammatory Agents to Treat COPD
发现治疗慢性阻塞性肺病的新型抗炎药
  • 批准号:
    9194162
  • 财政年份:
    2016
  • 资助金额:
    $ 4.68万
  • 项目类别:
Synthesis of anti-inflammatory agents and their structure-activity relationships studies
抗炎药的合成及其构效关系研究
  • 批准号:
    496858-2016
  • 财政年份:
    2016
  • 资助金额:
    $ 4.68万
  • 项目类别:
    University Undergraduate Student Research Awards
NAAA Inhibitors as Anti-inflammatory Agents, Phase II
NAAA 抑制剂作为抗炎剂,II 期
  • 批准号:
    9201955
  • 财政年份:
    2015
  • 资助金额:
    $ 4.68万
  • 项目类别:
Novel flavonoids as anti-inflammatory agents in alcoholism
新型黄酮类化合物作为酒精中毒的抗炎剂
  • 批准号:
    8251289
  • 财政年份:
    2014
  • 资助金额:
    $ 4.68万
  • 项目类别:
TLR-7 Agonists as Targeted Anti-inflammatory Agents in Arthritis
TLR-7 激动剂作为关节炎的靶向抗炎药
  • 批准号:
    8302750
  • 财政年份:
    2012
  • 资助金额:
    $ 4.68万
  • 项目类别:
Design and in vivo delivery of novel anti-inflammatory agents
新型抗炎剂的设计和体内递送
  • 批准号:
    267940
  • 财政年份:
    2012
  • 资助金额:
    $ 4.68万
  • 项目类别:
    Operating Grants
Development of inlammasome inhibitors to be used as anti-inflammatory agents
开发用作抗炎剂的inlammasome抑制剂
  • 批准号:
    8403458
  • 财政年份:
    2012
  • 资助金额:
    $ 4.68万
  • 项目类别:
TLR-7 Agonists as Targeted Anti-inflammatory Agents in Arthritis
TLR-7 激动剂作为关节炎的靶向抗炎药
  • 批准号:
    8472443
  • 财政年份:
    2012
  • 资助金额:
    $ 4.68万
  • 项目类别:
Development of inlammasome inhibitors to be used as anti-inflammatory agents
开发用作抗炎剂的inlammasome抑制剂
  • 批准号:
    8549297
  • 财政年份:
    2012
  • 资助金额:
    $ 4.68万
  • 项目类别:
{{ showInfoDetail.title }}

作者:{{ showInfoDetail.author }}

知道了