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RISS 인기검색어
- 검색키워드
- 저자 : Sim Hyun-Jaung (검색결과 3 건)
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Sim, Hyun-Jaung,Kim, Min-Hye,Bhattarai, Govinda,Hwang, Jae-Won,So, Han-Sol,Poudel, Sher Bahadur,Cho, Eui-Sic,Kook, Sung-Ho,Lee, Jeong-Chae Korean Society for Molecular and Cellular Biology 2021 Molecules and cells Vol.44 No.4
Numerous studies highlight the potential benefits potentials of supplemental cartilage oligomeric matrix protein-angiopoietin-1 (COMP-Ang1) through improved angiogenic effects. However, our recent findings show that excessive overexpression of COMP-Ang1 induces an impaired bone marrow (BM) microenvironment and senescence of hematopoietic stem cells (HSCs). Here, we investigated the underlying mechanisms of how excessive COMP-Ang1 affects the function of BM-conserved stem cells and hematopoiesis using K14-Cre;inducible-COMP-Ang1-transgenic mice. Excessive COMP-Ang1 induced peripheral egression and senescence of BM HSCs and mesenchymal stem cells (MSCs). Excessive COMP-Ang1 also caused abnormal hematopoiesis along with skewed differentiation of HSCs toward myeloid lineage rather than lymphoid lineage. Especially, excessive COMP-Ang1 disturbed late-stage erythroblast maturation, followed by decreased expression of stromal cell-derived factor 1 (SDF-1) and globin transcription factor 1 (GATA-1) and increased levels of superoxide anion and p-p38 kinase. However, transplantation with the mutant-derived BM cells or treatment with rhCOMP-Ang1 protein did not alter the frequency or GATA-1 expression of erythroblasts in recipient mice or in cultured BM cells. Together, our findings suggest that excessive COMP-Ang1 impairs the functions of BM HSCs and MSCs and hematopoietic processes, eventually leading to abnormal erythropoiesis via imbalanced SDF-1/CXCR4 axis and GATA-1 expression rather than Ang1/Tie2 signaling axis alterations.
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Genetic overexpression of COMP-Ang1 impairs BM microenvironment and induces senescence of BM HSCs
Kook, Sung-Ho,Sim, Hyun-Jaung,Hwang, Jae-Won,Baek, Young-Hyun,Kim, Chun-Chu,Lee, Jeong-Hoon,Cho, Eui-Sic,Lee, Jeong-Chae Elsevier 2018 Biochemical and biophysical research communication Vol.499 No.3
<P><B>Abstract</B></P> <P>Supplemental Angiopoietin 1 (Ang1) exerts its therapeutic potential on microvascular regression-associated diseases, and this potential is linked with the function of hematopoietic stem cells (HSCs). However, the underlying mechanisms of the effect of enhanced angiogenesis on the modulation of HSCs are not yet defined. Here, we generated transgenic mice expressing <B>C</B>artilage <B>O</B>ligomeric <B>M</B>atrix <B>P</B>rotein (COMP)-Ang1 in keratin 14-expressing cells. The mutant animals expressed excessive angiogenic characteristics in the skin and bone marrow (BM) along with redder skin with more numerous and branched vessels compared with their wild-type (WT) littermates. The mutants displayed reduced long bone formation and osteoclast activity than did WT littermates and had fewer CD150<SUP>+</SUP>CD48<SUP>−</SUP> <B>L</B>ineage<SUP>−</SUP> <B>S</B>ca-1<SUP>+</SUP>c-<B>K</B>it<SUP>+</SUP> (LSK) cells in the BM. The mutants also exhibited greater senescence-associated (SA) β-gal activity, p16<SUP>INK4a</SUP> protein expression, and superoxide anion levels in CD150<SUP>+</SUP>CD48<SUP>−</SUP>LSK cells in the BM. Furthermore, transplantation assay revealed that the mutant-derived LSK cells were inferior to the cells derived from WT littermate in inducing competitive repopulating capacity in the recipients. Collectively, our results demonstrate that persistent and prolonged administration of COMP-Ang1 by inducible transgenic expression mediates excessive angiogenesis in the body and impairs BM microenvironment, eventually leading to senescence of BM HSCs.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Transgenic mice expressing COMP-Ang1 in keratin 14-expressing cells were generated. </LI> <LI> The mutant expressed excessive angiogenic characteristics in the skin and BM. </LI> <LI> The mutants displayed impaired BM microenvironment with low osteoclast activity. </LI> <LI> Collectively, genetic COMP-Ang1 overexpression induces senescence of BM HSCs. </LI> </UL> </P>
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Bhattarai Govinda,Shrestha Saroj Kumar,Sim Hyun-Jaung,Lee Jeong-Chae,Kook Sung-Ho 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
The harmful effects of fine particulate matter ≤2.5 µm in size (PM2.5) on human health have received considerable attention. However, while the impact of PM2.5 on the respiratory and cardiovascular systems has been well studied, less is known about the effects on stem cells in the bone marrow (BM). With an emphasis on the invasive characteristics of PM2.5, this review examines the current knowledge of the health effects of PM2.5 exposure on BM-residing stem cells. Recent studies have shown that PM2.5 enters the circulation and then travels to distant organs, including the BM, to induce oxidative stress, systemic inflammation and epigenetic changes, resulting in the reduction of BM-residing stem cell survival and function. Understanding the broader health effects of air pollution thus requires an understanding of the invasive characteristics of PM2.5 and its direct influence on stem cells in the BM. As noted in this review, further studies are needed to elucidate the underlying processes by which PM2.5 disturbs the BM microenvironment and inhibits stem cell functionality. Strategies to prevent or ameliorate the negative effects of PM2.5 exposure on BM-residing stem cells and to maintain the regenerative capacity of those cells must also be investigated. By focusing on the complex relationship between PM2.5 and BM-resident stem cells, this review highlights the importance of specific measures directed at safeguarding human health in the face of rising air pollution.
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