Relationship Between Keloid Pathogenesis and Endothelial Progenitor Cells: A Review Study

Context: Keloid scars are disfiguring lesions (ie, reddish-brown bulges on the skin surface) formed after a minor injury or surgical invasion. They lead to severe itching or pain, thereby causing physical and psychological distress in patients. Evidence Acquisition: Scholarly databases, including Web of Science, PubMed, and Google Scholar, were searched for relevant articles using keywords such as “keloids,” “endothelial progenitor cells” (EPCs), and “CD34-positive cells.” Results: Keloid scars are classified as an intractable disease; their cause is unknown, and there is no specific therapy. Their pathogenic effects on inflammation around wounds and fibroblasts have been extensively studied. However, details regarding their onset mechanism and definitive factors that contribute to their formation have not yet been elucidated. Adult stem cell therapy, especially regenerative therapy aimed at recovering tissue structure and function, has been extensively studied globally. In our recently published study, we identified an association between keloid scar development and EPCs. However, there is still no systematic review in this regard. Conclusions: This paper provides information on preventing keloids and further understanding the cause of this disease by reviewing previous studies on the association between keloids and EPCs.

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Regulatory effect of dimethylarginine dimethylaminohydrolase on endothelial progenitor cells differentiation and function

Cell Biology International ◽

10.1042/cbi034s042b ◽

2010 ◽

Vol 34 (8) ◽

pp. S42-S42

Author(s):

Qiong Yuan ◽

Chang‑Ping Hu ◽

Si‑Yu Liu ◽

Xu‑Meng Chen ◽

Jun Peng ◽

...

Keyword(s):

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Regulatory Effect ◽

Dimethylarginine Dimethylaminohydrolase ◽

Endothelial Progenitor ◽

And Function

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Quantitative and functional evaluation of endothelial progenitor cells in patients with cardiac amyloidosis

European Heart Journal ◽

10.1093/ehjci/ehaa946.2114 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

O Itzhaki Ben Zadok ◽

D Leshem-Lev ◽

T Ben-Gal ◽

A Hamdan ◽

N Schamroth-Pravda ◽

...

Keyword(s):

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Mtt Assay ◽

Cardiac Amyloidosis ◽

Microvascular Dysfunction ◽

Functional Evaluation ◽

Endothelial Progenitor ◽

Colony Forming Units ◽

Study Population ◽

And Function

Abstract Background Endothelial microvascular dysfunction is a known mechanism of injury in cardiac amyloidosis (CA), but evidence regarding the level and function of endothelial progenitor cells (EPCs) in patients with CA is lacking. Methods Study population included patients with light-chain or transthyretin (ATTR) CA. Patients with diagnosed heart failure and preserved ejection fraction (HFpEF) without monoclonal gammopathy and a 99mTc-DPD scan incompatible with TTR were used as controls. Blood circulating EPCs were assessed quantitatively by the expression of VEGFR-2(+), CD34(+) and CD133(+) using flow cytometry, and functionally by the formation of colony forming units (CFUs). MTT assay was used to demonstrate cell viability. Tests were repeated 3 months following the initiation of amyloid-suppressive therapies (either ATTR-stabilizer or targeted chemotherapy) in CA patients. Results Our preliminary cohort included 14 CA patients (median age 74 years, 62% ATTR CA). Patients with CA vs. patients with HFpEF (n=8) demonstrated lower expression of CD34(+)/VEGFR-2(+) cells [0.51% (IQR 0.4, 0.7) vs. 1.03% (IQR 0.6, 1.4), P=0.043] and CD133(+)/VEGFR-2(+) cells [0.35% (IQR 0.23, 0.52) to 1.07% (IQR 0.6, 1.5), P=0.003]. Functionally, no differences were noted between groups. Following the initiation of amyloid-suppressive therapies in CA patients, we observed the up-regulation of CD34(+)/VEGFR-2(+) cells [2.47% (IQR 2.1, 2.7), P<0.001] and CD133(+)/VEGFR-2(+) cells [1.38% (IQR 1.1, 1.7), P=0.003]. Moreover, functionally, active EPCs were evident microscopically by their ability to form colonies (from 0.5 CFUs [IQR 0, 1.5) to 2 CFUs (IQR 1, 3.5), P=0.023]. EPCs' viability was demonstrated by an MTT assay [0.12 (IQR 0.04, 0.12) to 0.24 (IQR 0.16, 0.3), p=0.014]. Conclusions These preliminary results demonstrate reduced EPCs levels in CA patients indicating significant microvascular impairment. Amyloid-targeted therapies induce the activation of EPCs, thus possibly promoting endothelial regeneration. These findings may represent a novel mechanism of action of amyloid-suppressive therapies EPCs in CA patients and during therapy Funding Acknowledgement Type of funding source: None

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Correction: Period2 Deficiency Blunts Hypoxia-Induced Mobilization and Function of Endothelial Progenitor Cells

PLoS ONE ◽

10.1371/journal.pone.0119196 ◽

2015 ◽

Vol 10 (3) ◽

pp. e0119196

Author(s):

Keyword(s):

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Endothelial Progenitor ◽

And Function

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Decreased Count and Dysfunction of Circulating EPCs in Postmenopausal Hypercholesterolemic Females via Reducing NO Production

Stem Cells International ◽

10.1155/2018/2543847 ◽

2018 ◽

Vol 2018 ◽

pp. 1-10 ◽

Cited By ~ 1

Author(s):

Ying Luo ◽

Quan-Neng Yan ◽

Wan-Zhou Wu ◽

Fan-Yan Luo

Keyword(s):

Endothelial Dysfunction ◽

Progenitor Cells ◽

Endothelial Progenitor Cells ◽

Therapeutic Strategy ◽

No Production ◽

Endothelial Progenitor ◽

Endothelial Repair ◽

Flow Mediated Dilatation ◽

Premenopausal Female ◽

And Function

Endothelial progenitor cells (EPCs) contribute to the endogenous endothelial repair program during hypercholesterolemia. EPC count and migratory and proliferative capacities remain unchanged in the premenopausal female with hypercholesterolemia. However, the changes of count and activity of circulating EPCs in the hypercholesterolemic postmenopausal females are unknown. Here, we find that the migratory and proliferative capacities of circulating EPCs were decreased in patients with hypercholesterolemia versus normocholesterolemia. No significant differences were found between postmenopausal females and age-matched males. NO production showed positive correlation with the activity and count of circulating EPCs in patients with hypercholesterolemia. Flow-mediated dilatation (FMD) is directly interrelated with EPC counts and function. Our findings reveal that decreased EPC count and endothelial dysfunction lead to less NO production in hypercholesterolemic postmenopausal females. Maintaining the EPC numbers and activity might be emerging as a potential therapeutic strategy to reduce the risk of cardiovascular injury in elder women.

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