scholarly journals Tissue Repair and Regeneration after Lung Injury: The Role of Bone Marrow —Derived Cells

2005 ◽  
Vol 25 (3) ◽  
pp. 293-300
Author(s):  
Hiroshi KUBO
Keyword(s):  
Bone Marrow ◽  
Lung Injury ◽  
Tissue Repair ◽  
Tissue Repair And Regeneration

scholarly journals Leukocyte immunoglobulin-like receptor B4 deficiency exacerbates acute lung injury via NF-κB signaling in bone marrow-derived macrophages

2019 ◽  
Vol 39 (6) ◽  
Author(s):  
Tao Qiu ◽  
Jiangqiao Zhou ◽  
Tianyu Wang ◽  
Zhongbao Chen ◽  
Xiaoxiong Ma ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Stromal Cells ◽  
Marrow Cell ◽  
Marrow Transplant ◽  
Cell Source ◽  
Transplant Model ◽  
Acute Inflammatory Disease

AbstractAcute lung injury (ALI) is an acute inflammatory disease. Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing inhibitory receptor that is implicated in various pathological processes. However, the function of LILRB4 in ALI remains largely unknown. The aim of the present study was to explore the role of LILRB4 in ALI. LILRB4 knockout mice (LILRB4 KO) were used to construct a model of ALI. Bone marrow cell transplantation was used to identify the cell source of the LILRB4 deficiency-aggravated inflammatory response in ALI. The effect on ALI was analyzed by pathological and molecular analyses. Our results indicated that LILRB4 KO exacerbated ALI triggered by LPS. Additionally, LILRB4 deficiency can enhance lung inflammation. According to the results of our bone marrow transplant model, LILRB4 regulates the occurrence and development of ALI by bone marrow-derived macrophages (BMDMs) rather than by stromal cells in the lung. The observed inflammation was mainly due to BMDM-induced NF-κB signaling. In conclusion, our study demonstrates that LILRB4 deficiency plays a detrimental role in ALI-associated BMDM activation by prompting the NF-κB signal pathway.

scholarly journals Role of prostaglandin E2 in tissue repair and regeneration

Theranostics ◽  
2021 ◽  
Vol 11 (18) ◽  
pp. 8836-8854
Author(s):  
Hui Cheng ◽  
Haoyan Huang ◽  
Zhikun Guo ◽  
Ying Chang ◽  
Zongjin Li
Keyword(s):  
Prostaglandin E2 ◽  
Tissue Repair ◽  
Tissue Repair And Regeneration

Abstract 13: Plasminogen Is Required for Hematopoietic Stem Cell-Mediated Cardiac Repair After Myocardial Infarction

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Yanqing Gong ◽  
Jane Hoover-Plow ◽  
Ying Li
Keyword(s):  
Myocardial Infarction ◽  
Stem Cells ◽  
Bone Marrow ◽  
Stem Cell ◽  
Tissue Repair ◽  
Critical Role ◽  
Cardiac Repair ◽  
Internal Diameter ◽  
Hematopoietic Stem

Ischemic heart disease, including myocardial infarction (MI), is the primary cause of death throughout the US. Granulocyte colony-stimulating factor (G-CSF) is used to mobilize hematopoietic progenitor and stem cells (HPSC) to improve cardiac recovery after MI. However, poor-mobilization to G-CSF is observed in 25% of patients and 10-20% of healthy donors. Therefore, a better understanding of the underlying mechanisms regulating G-CSF-induced cardiac repair may offer novel approaches for strengthening stem cell-mediated therapeutics. Our previous studies have identified an essential role of Plg in HPSC mobilization from bone marrow (BM) in response to G-CSF. Here, we investigate the role of Plg in G-CSF-stimulated cardiac repair after MI. Our data show that G-CSF significantly improves cardiac tissue repair including increasing neovascularization in the infarct area, and improving ejection fraction and LV internal diameter by echocardiogram in wild-type mice. No improvement in tissue repair and heart function by G-CSF is observed in Plg -/- mice, indicating that Plg is required for G-CSF-regulated cardiac repair after MI. To investigate whether Plg regulates HPSC recruitment to ischemia area, bone marrow transplantion (BMT) with EGFP-expressing BM cells was performed to visualize BM-derived stem cells in infarcted tissue. Our data show that G-CSF dramatically increases recruitment of GFP+ cells (by 16 fold) in WT mice but not in Plg -/- mice, suggesting that Plg is essential for HPSC recruitment from BM to the lesion sites after MI. In further studies, we investigated the role of Plg in the regulation of SDF-1/CXCR-4 axis, a major regulator for HPSC recruitment. Our results show that G-CSF significantly increases CXCR-4 expression in infarcted area in WT mice. While G-CSF-induced CXCR-4 expression is markedly decreased (80%) in Plg -/- mice, suggesting Plg may regulate CXCR-4 expression during HSPC recruitment to injured heart. Interestingly, Plg does not affect SDF-1 expression in response to G-CSF treatment. Taken together, our findings have identified a critical role of Plg in HSPC recruitment to the lesion site and subsequent tissue repair after MI. Thus, targeting Plg may offer a new therapeutic strategy to improve G-CSF-mediated cardiac repair after MI.

scholarly journals Wnt signaling in kidney: the initiator or terminator?

2020 ◽  
Vol 98 (11) ◽  
pp. 1511-1523 ◽  
Author(s):  
Ping Meng ◽  
Mingsheng Zhu ◽  
Xian Ling ◽  
Lili Zhou
Keyword(s):  
Cell Differentiation ◽  
Embryonic Development ◽  
Wnt Signaling ◽  
Tissue Repair ◽  
Progenitor Cell ◽  
Kidney Development ◽  
Kidney Diseases ◽  
Electrolyte Balance ◽  
Tissue Repair And Regeneration

Abstract The kidney is a key organ in the human body that excretes toxins and sustains the water–electrolyte balance. During embryonic development and disease progression, the kidney undergoes enormous changes in macrostructure, accompanied by a variety of microstructural histological changes, such as glomerular formation and sclerosis, tubule elongation and atrophy, interstitial establishment, and fibrosis progression. All of these rely on the frequent occurrence of cell death and growth. Notably, to overcome disease, some cells regenerate through self-repair or progenitor cell differentiation. However, the signaling mechanisms underlying kidney development and regeneration have not been elucidated. Recently, Wnt signaling has been noted to play an important role. Although it is a well-known developmental signal, the role of Wnt signaling in kidney development and regeneration is not well recognized. In this review, we review the role of Wnt signaling in kidney embryonic development, tissue repair, cell division, and progenitor cell differentiation after injury. Moreover, we briefly highlight advances in our understanding of the pathogenic mechanisms of Wnt signaling in mediating cellular senescence in kidney parenchymal and stem cells, an irreversible arrest of cell proliferation blocking tissue repair and regeneration. We also highlight the therapeutic targets of Wnt signaling in kidney diseases and provide important clues for clinical strategies.

scholarly journals Regulatory Effect of Mesenchymal Stem Cells on T Cell Phenotypes in Autoimmune Diseases

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Zhiping Wei ◽  
Jintao Yuan ◽  
Gaoying Wang ◽  
Dickson Kofi Wiredu Ocansey ◽  
Zhiwei Xu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
T Cell ◽  
Autoimmune Diseases ◽  
Tissue Repair ◽  
T Cell Subsets ◽  
Autoimmune Conditions ◽  
T Cell Phenotypes ◽  
Cell Phenotypes

Research on mesenchymal stem cells (MSCs) starts from the earliest assumption that cells derived from the bone marrow have the ability to repair tissues. Several scientists have since documented the crucial role of bone marrow-derived MSCs (BM-MSCs) in processes such as embryonic bone and cartilage formation, adult fracture and tissue repair, and immunomodulatory activities in therapeutic applications. In addition to BM-MSCs, several sources of MSCs have been reported to possess tissue repair and immunoregulatory abilities, making them potential treatment options for many diseases. Therefore, the therapeutic potential of MSCs in various diseases including autoimmune conditions has been explored. In addition to an imbalance of T cell subsets in most patients with autoimmune diseases, they also exhibit complex disease manifestations, overlapping symptoms among diseases, and difficult treatment. MSCs can regulate T cell subsets to restore their immune homeostasis toward disease resolution in autoimmune conditions. This review summarizes the role of MSCs in relieving autoimmune diseases via the regulation of T cell phenotypes.

Anti-Inflammatory and Immunomodulatory Role of Bone Marrow-Derived MSCs in Mice with Acute Lung Injury

2021 ◽  
Vol 41 (1) ◽  
pp. 29-36
Author(s):  
Mohamed Abdelmoneim ◽  
El-Sayed Y. El-Naenaeey ◽  
Somia Hassan Abd-Allah ◽  
Ahlam A. Gharib ◽  
Mona Alhussein ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Anti Inflammatory

The role of cellular senescence in tissue repair and regeneration

2021 ◽  
pp. 111528
Author(s):  
Lucía Antelo-Iglesias ◽  
Pilar Picallos-Rabina ◽  
Valentín Estévez-Souto ◽  
Sabela Da Silva-Álvarez ◽  
Manuel Collado
Keyword(s):  
Cellular Senescence ◽  
Tissue Repair ◽  
Tissue Repair And Regeneration

scholarly journals The Role of Therapeutic Angiogenesis in Tissue Repair and Regeneration

2005 ◽  
Vol 18 (9) ◽  
pp. 501-502 ◽  
Author(s):  
William W. Li ◽  
Katherine Talcott ◽  
Amy Zhai ◽  
Erwin A. Kruger ◽  
Vincent W. Li
Keyword(s):  
Tissue Repair ◽  
Therapeutic Angiogenesis ◽  
Tissue Repair And Regeneration
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