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The loss-of-function and gain-of-function of MYSM1 were evaluated in H/R-treated cardiomyocyte. A-D. MYSM1 knockdown (KD) HL-1 cells were constructed via shRNA (shMYSM1) before H/R injury (4 h of hypoxia and 6 h of reoxygenation). (A) Cell viability was assessed using the CCK8 assay (n = 6). (B) Bar graph showing the levels of LDH (n = 6). (C, D) The effect of MYSM1 knockdown on H/R-induced apoptosis in HL-1 determined by PI staining. Representative images for PI staining are shown (D), with quantitative columns for PI-positive cells (C, n = 6). E-H. MYSM1 was overexpressed by transfecting HL-1 cells with Flag-MYSM1 (oeMYSM1) before H/R injury. (E) Cell viability was assessed using the CCK8 assay (n = 6). (F) Bar graph showing the levels of LDH (n = 6). (G-H) The effect of oeMYSM1 on H/R-induced apoptosis in HL-1 determined by PI staining. Representative images for PI staining are shown (H), with quantitative columns for PI-positive cells (G, n = 6). I-L. MYSM1 was knocked down by siRNA transfection (siMYSM1) in NRPCs before H/R injury. (I) Cell viability was assessed using the CCK8 assay (n = 6). (J) Bar graph showing the levels of LDH (n = 6). (K-L) The effect of siMYSM1 on H/R-induced apoptosis in NRPCs was determined by PI staining. Representative images for PI staining are shown (L), with quantitative columns for PI-positive cells (K, n = 6). (* P < 0.05, ** P < 0.01, *** P < 0.001).
Source publication
Rationale: Myocardial ischemia/reperfusion (I/R) injury leads to irreversible cardiomyocyte death and aggravates myocardial infarction. Deubiquitinating enzymes (DUBs) are essential for maintaining substrate protein stability and functionality, playing significant roles in cardiac pathophysiology. In this study, we aimed to clarify the regulatory r...
Contexts in source publication
Context 1
... previous data suggested that MYSM1 knockdown protected against myocardial I/R injury, with MYSM1 expression mainly upregulated in I/R-stimulated cardiomyocytes. To further explore the role of MYSM1 in vitro, the MYSM1-knockdown (MYSM1-KD) HL-1 cells were constructed via shRNA (shMYSM1, Figure S4A). Notably, MYSM1 knockdown significantly enhanced cell viability ( Figure 4A) and inhibited the activity of LDH in the cellular supernatant ( Figure 4B) under H/R injury. ...
Context 2
... further explore the role of MYSM1 in vitro, the MYSM1-knockdown (MYSM1-KD) HL-1 cells were constructed via shRNA (shMYSM1, Figure S4A). Notably, MYSM1 knockdown significantly enhanced cell viability ( Figure 4A) and inhibited the activity of LDH in the cellular supernatant ( Figure 4B) under H/R injury. Additionally, MYSM1 knockdown reduced the quantity of Propidium Iodide (PI)-positive nuclei during H/R injury (Figure 4C-D). ...
Context 3
... further explore the role of MYSM1 in vitro, the MYSM1-knockdown (MYSM1-KD) HL-1 cells were constructed via shRNA (shMYSM1, Figure S4A). Notably, MYSM1 knockdown significantly enhanced cell viability ( Figure 4A) and inhibited the activity of LDH in the cellular supernatant ( Figure 4B) under H/R injury. Additionally, MYSM1 knockdown reduced the quantity of Propidium Iodide (PI)-positive nuclei during H/R injury (Figure 4C-D). ...
Context 4
... MYSM1 knockdown significantly enhanced cell viability ( Figure 4A) and inhibited the activity of LDH in the cellular supernatant ( Figure 4B) under H/R injury. Additionally, MYSM1 knockdown reduced the quantity of Propidium Iodide (PI)-positive nuclei during H/R injury (Figure 4C-D). The effect of siMYSM1 on H/R-induced apoptosis in NRPCs was determined by PI staining. ...
Context 5
... a manner analogous to the assessment of loss-of-function, the gain-of-function of MYSM1 was evaluated by transfecting HL-1 cells with oeMYSM1 ( Figure S4B). Our study indicated that upregulation of MYSM1 led to decreased cellular viability ( Figure 4E) and elevated LDH release during H/R injury ( Figure 4F). ...
Context 6
... a manner analogous to the assessment of loss-of-function, the gain-of-function of MYSM1 was evaluated by transfecting HL-1 cells with oeMYSM1 ( Figure S4B). Our study indicated that upregulation of MYSM1 led to decreased cellular viability ( Figure 4E) and elevated LDH release during H/R injury ( Figure 4F). We further found that upregulation of MYSM1 increased the quantity of PI-positive nuclei following H/R injury (Figure 4G-H). ...
Context 7
... a manner analogous to the assessment of loss-of-function, the gain-of-function of MYSM1 was evaluated by transfecting HL-1 cells with oeMYSM1 ( Figure S4B). Our study indicated that upregulation of MYSM1 led to decreased cellular viability ( Figure 4E) and elevated LDH release during H/R injury ( Figure 4F). We further found that upregulation of MYSM1 increased the quantity of PI-positive nuclei following H/R injury (Figure 4G-H). ...
Context 8
... study indicated that upregulation of MYSM1 led to decreased cellular viability ( Figure 4E) and elevated LDH release during H/R injury ( Figure 4F). We further found that upregulation of MYSM1 increased the quantity of PI-positive nuclei following H/R injury (Figure 4G-H). ...
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... previously described, NRPCs were isolated from the left ventricles of neonatal SD rats [14], and MYSM1 was silenced by siRNA transfection (siMYSM1, Figure S4C). As shown in Figure 4I-J, MYSM1 silencing markedly increased cell viability (Figure 4I) and suppressed the LDH release ( Figure 4J) during H/R injury. ...
Context 10
... previously described, NRPCs were isolated from the left ventricles of neonatal SD rats [14], and MYSM1 was silenced by siRNA transfection (siMYSM1, Figure S4C). As shown in Figure 4I-J, MYSM1 silencing markedly increased cell viability (Figure 4I) and suppressed the LDH release ( Figure 4J) during H/R injury. Furthermore, MYSM1 silencing decreased PI-positive nuclei in H/R injury (Figure 4K-L). ...
Context 11
... previously described, NRPCs were isolated from the left ventricles of neonatal SD rats [14], and MYSM1 was silenced by siRNA transfection (siMYSM1, Figure S4C). As shown in Figure 4I-J, MYSM1 silencing markedly increased cell viability (Figure 4I) and suppressed the LDH release ( Figure 4J) during H/R injury. Furthermore, MYSM1 silencing decreased PI-positive nuclei in H/R injury (Figure 4K-L). ...
Context 12
... previously described, NRPCs were isolated from the left ventricles of neonatal SD rats [14], and MYSM1 was silenced by siRNA transfection (siMYSM1, Figure S4C). As shown in Figure 4I-J, MYSM1 silencing markedly increased cell viability (Figure 4I) and suppressed the LDH release ( Figure 4J) during H/R injury. Furthermore, MYSM1 silencing decreased PI-positive nuclei in H/R injury (Figure 4K-L). ...
Context 13
... shown in Figure 4I-J, MYSM1 silencing markedly increased cell viability (Figure 4I) and suppressed the LDH release ( Figure 4J) during H/R injury. Furthermore, MYSM1 silencing decreased PI-positive nuclei in H/R injury (Figure 4K-L). These results validated that MYSM1 contributes to H/R-induced cardiomyocyte injury in vitro. ...
