Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration

Krstić, Jelena; Obradović, Hristina; Jauković, Aleksandra; Okić-Đorđević, Ivana; Trivanović, Drenka; Кукољ, Тамара; Mojsilović, Slavko; Ilić, Vesna; Santibáñez, Juan F.; Bugarski, Diana

doi:10.1016/j.bbamcr.2014.11.025

Cited by 36 publications

(37 citation statements)

References 48 publications

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“…The PB MSC isolation was performed as previously described . Briefly, mononuclear cells were obtained from the PB of healthy donors by density gradient centrifugation on lymphocyte separation media (PAA Laboratories, Linz, Austria).…”

Section: Methodsmentioning

confidence: 99%

Hydroxyurea‐induced senescent peripheral blood mesenchymal stromal cells inhibit bystander cell proliferation of JAK2V617F‐positive human erythroleukemia cells

et al. 2019

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Hydroxyurea (HU) is a nonalkylating antineoplastic agent used in the treatment of hematological malignancies. HU is a DNA replication stress inducer, and as such, it may induce a premature senescence‐like cell phenotype; however, its repercussion on bystander cell proliferation has not been revealed so far. Our results indicate that HU strongly inhibited peripheral blood mesenchymal stromal cells (PBMSC) proliferation by cell cycle arrest in S phase, and that, consequently, PBMSC acquire senescence‐related phenotypical changes. HU‐treated PBMSC display increased senescence‐associated β‐galactosidase levels and p16INK4 expression, as well as DNA damage response and genotoxic effects, evidenced by expression of γH2A.X and micronuclei. Moreover, HU‐induced PBMSC senescence is mediated by increased reactive oxygen species (ROS) levels, as demonstrated by the inhibition of senescence markers in the presence of ROS scavenger N‐acetylcysteine and NADPH oxidase inhibitor Apocynin. To determine the HU‐induced bystander effect, we used the JAK2V617F‐positive human erythroleukemia 92.1.7 (HEL) cells. Co‐culture with HU‐induced senescent PBMSC (HU‐S‐PBMSC) strongly inhibited bystander HEL cell proliferation, and this effect is mediated by both ROS and transforming growth factor (TGF)‐β expression. Besides induction of premature senescence, HU educates PBMSC toward an inhibitory phenotype of HEL cell proliferation. Finally, our study contributes to the understanding of the role of HU‐induced PBMSC senescence as a potential adjuvant in hematological malignancy therapies.

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Section: Methodsmentioning

confidence: 99%

Hydroxyurea‐induced senescent peripheral blood mesenchymal stromal cells inhibit bystander cell proliferation of JAK2V617F‐positive human erythroleukemia cells

et al. 2019

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“…Urokinase‐type plasminogen activator (PA) has been found in MSC protrusions (Fig. ) and can support migration of MSCs under ERK 1,2 MAPK signaling . Overcoming the endothelial basement barrier by MSCs involves proteases including collagenases and metalloproteinases such as Matrix metalloprotease 2 (MMP‐2).…”

Section: Priming and Requirements For Extravasationmentioning

confidence: 99%

Concise Review: MSC Adhesion Cascade—Insights into Homing and Transendothelial Migration

et al. 2017

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Mesenchymal stem cells (MSCs) are promising candidates for adult cell therapies in regenerative medicine. To fully exert their potential, efficient homing and migration toward lesion sites play an important role. Local transplantation deposits MSC in spatial proximity to the lesion, but often requires invasive procedures. Systemic administration routes are favored, but require the targeted extravasation of the circulating MSC at the site of injury. Transplanted MSC can indeed leave the blood flow and transmigrate through the endothelial barrier, and reach the lesion site. However, the underlying processes are not completely dissolved yet. Recent in vitro and in vivo research identified some key molecules scattered light on the extravasation mechanism. This review provides a detailed overview over the current knowledge of MSC transendothelial migration. We use the leukocyte extravasation process as a role model to build a comprehensive concept of MSC egress mechanisms from the blood stream and identified relevant similarities as well as important differences between the extravasation mechanisms. Stem Cells 2017;35:1446-1460.

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“…MSCs can be obtained from different adult tissues such as bone marrow2, adipose tissue3, umbilical blood4, umbilical cord5 and peripheral blood6. Adipose-derived mesenchymal stem cells (ADMSCs) have one big advantage over other tissue-derived MSCs in that they are easily accessible.…”

mentioning

confidence: 99%

CD61 promotes the differentiation of canine ADMSCs into PGC-like cells through modulation of TGF-β signaling

Fang

Wei

et al. 2017

Sci Rep

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Previous studies have shown that CD61 (integrin-β3) promotes the differentiation of human umbilical cord mesenchymal stem cells (hUC-MSCs) into germ-like cells. However, the mechanism remains unclear. In this study, we showed that overexpression of CD61 in canine adipose-derived mesenchymal stem cells (cADMSCs) promotes their differentiation into primordial germ cell (PGC)-like cells. Quantitative real-time PCR, immunocytochemistry and western blot detected higher levels of PGC-specific markers in CD61-overexpressed cADMSCs compared with those in control cells. Moreover, phosphorylation of Smad2, a downstream mediator of transforming growth factor beta (TGF-β), was increased in CD61-overexpressed cADMSCs than that in control cells. However, the expression of PGC-specific markers was downregulated in cADMSCs treated with a TGF-β inhibitor. These results suggested that CD61 could induce cADMSCs to differentiate into PGC-like cells by relying on the activation of TGF-β pathway. ADMSCs possess a considerable potential in treating the infertility of rare animal species.

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Urokinase type plasminogen activator mediates Interleukin-17-induced peripheral blood mesenchymal stem cell motility and transendothelial migration

Cited by 36 publications

References 48 publications

Hydroxyurea‐induced senescent peripheral blood mesenchymal stromal cells inhibit bystander cell proliferation of JAK2V617F‐positive human erythroleukemia cells

Hydroxyurea‐induced senescent peripheral blood mesenchymal stromal cells inhibit bystander cell proliferation of JAK2V617F‐positive human erythroleukemia cells

Concise Review: MSC Adhesion Cascade—Insights into Homing and Transendothelial Migration

CD61 promotes the differentiation of canine ADMSCs into PGC-like cells through modulation of TGF-β signaling

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