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$Cardiac regenerating islet‐derived 3 γ <t>(Reg3</t> γ ) gene expression in hypertrophied hearts and after myocardial infarction. Left ventricular <t>Reg3</t> <t>γ</t> gene expression in spontaneously hypertensive rats (SHR) and in their age‐matched controls Wistar Kyoto rats (WKY). (A) White columns, WKY; black columns, SHR. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 4–11). *** P < 0.001 20‐month‐old SHR versus age‐matched WKY rats (Student's t ‐test). The effect of myocardial infarction (MI) on left ventricular Reg3 γ mRNA (B) and protein (C) levels in rats after 1 day and 2 weeks after MI. Reg3 γ was observed at 17 kDa, the values were normalized to GAPDH (36 kDa, total protein fraction), representative Western blots are shown. The controls went through the same invasive operation without the ligation of left anterior descending coronary artery. White columns, control; black columns, myocardial infarction. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA and total protein levels were assessed by Western blot analyses. Results are expressed as mean ± SEM ( n = 5–8). *** P < 0.001, ** P < 0.01, infarct versus control (Student's t ‐test).$
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1) Product Images from "Mitogen‐activated protein kinase p38 target regenerating islet‐derived 3 γ expression is upregulated in cardiac inflammatory response in the rat heart"

Article Title: Mitogen‐activated protein kinase p38 target regenerating islet‐derived 3 γ expression is upregulated in cardiac inflammatory response in the rat heart

Journal: Physiological Reports

doi: 10.14814/phy2.12996

$Cardiac regenerating islet‐derived 3 γ (Reg3 γ ) gene expression in hypertrophied hearts and after myocardial infarction. Left ventricular Reg3 γ gene expression in spontaneously hypertensive rats (SHR) and in their age‐matched controls Wistar Kyoto rats (WKY). (A) White columns, WKY; black columns, SHR. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 4–11). *** P < 0.001 20‐month‐old SHR versus age‐matched WKY rats (Student's t ‐test). The effect of myocardial infarction (MI) on left ventricular Reg3 γ mRNA (B) and protein (C) levels in rats after 1 day and 2 weeks after MI. Reg3 γ was observed at 17 kDa, the values were normalized to GAPDH (36 kDa, total protein fraction), representative Western blots are shown. The controls went through the same invasive operation without the ligation of left anterior descending coronary artery. White columns, control; black columns, myocardial infarction. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA and total protein levels were assessed by Western blot analyses. Results are expressed as mean ± SEM ( n = 5–8). *** P < 0.001, ** P < 0.01, infarct versus control (Student's t ‐test).$
Figure Legend Snippet: Cardiac regenerating islet‐derived 3 γ (Reg3 γ ) gene expression in hypertrophied hearts and after myocardial infarction. Left ventricular Reg3 γ gene expression in spontaneously hypertensive rats (SHR) and in their age‐matched controls Wistar Kyoto rats (WKY). (A) White columns, WKY; black columns, SHR. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 4–11). *** P < 0.001 20‐month‐old SHR versus age‐matched WKY rats (Student's t ‐test). The effect of myocardial infarction (MI) on left ventricular Reg3 γ mRNA (B) and protein (C) levels in rats after 1 day and 2 weeks after MI. Reg3 γ was observed at 17 kDa, the values were normalized to GAPDH (36 kDa, total protein fraction), representative Western blots are shown. The controls went through the same invasive operation without the ligation of left anterior descending coronary artery. White columns, control; black columns, myocardial infarction. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA and total protein levels were assessed by Western blot analyses. Results are expressed as mean ± SEM ( n = 5–8). *** P < 0.001, ** P < 0.01, infarct versus control (Student's t ‐test).

Techniques Used: Derivative Assay, Gene Expression, Northern Blot, Western Blot, Ligation, Control

Angiotensin II (Ang II) regulates cardiac regenerating islet‐derived 3 γ (Reg3 γ ) gene expression. The effect of subcutaneous administration of Ang II via osmotic minipumps for 6, 12, and 72 h, and 2 weeks on left ventricular Reg3 γ mRNA levels (A). White columns, control; black columns, Ang II. (B) The effect of subcutaneous administration of Ang II, losartan (Los) and their combination for 6 h on left ventricular Reg3 γ mRNA levels. White columns, control (ctrl); black columns, Ang II; dark gray column, Ang II + Los; light gray column, Los. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 6–9). * P < 0.05, ** P < 0.01, *** P < 0.001, Ang II versus control (ctrl), ## P < 0.01 Ang II + losartan versus Ang II (One‐way ANOVA followed by a least significant difference post hoc test). Representative images demonstrating cardiac Reg3 γ (C, D) and alpha smooth muscle actin ( α ‐SMA) (E, F) expression in rats after 6 h‐infusion of Ang II. Control (ctrl) (C, E); Ang II (D, F). Magnification 100×, scale bar 100 μ mol L −1 .

Figure Legend Snippet: Angiotensin II (Ang II) regulates cardiac regenerating islet‐derived 3 γ (Reg3 γ ) gene expression. The effect of subcutaneous administration of Ang II via osmotic minipumps for 6, 12, and 72 h, and 2 weeks on left ventricular Reg3 γ mRNA levels (A). White columns, control; black columns, Ang II. (B) The effect of subcutaneous administration of Ang II, losartan (Los) and their combination for 6 h on left ventricular Reg3 γ mRNA levels. White columns, control (ctrl); black columns, Ang II; dark gray column, Ang II + Los; light gray column, Los. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 6–9). * P < 0.05, ** P < 0.01, *** P < 0.001, Ang II versus control (ctrl), ## P < 0.01 Ang II + losartan versus Ang II (One‐way ANOVA followed by a least significant difference post hoc test). Representative images demonstrating cardiac Reg3 γ (C, D) and alpha smooth muscle actin ( α ‐SMA) (E, F) expression in rats after 6 h‐infusion of Ang II. Control (ctrl) (C, E); Ang II (D, F). Magnification 100×, scale bar 100 μ mol L −1 .

Techniques Used: Derivative Assay, Gene Expression, Control, Northern Blot, Expressing

$Regulation of regenerating islet‐derived 3 γ (Reg3 γ ) expression in cultured neonatal rat ventricular myocytes. Ventricular myocytes were exposed to lipopolysaccharide (LPS) (A, B) endothelin‐1 (ET‐1) (C) and fibroblast growth factor ‐1 (FGF‐1) (D) for 4–24 h ( n = 12–18). (E) Ventricular myocytes were exposed to cyclic mechanical stretch, in which the frequency of stretching was 0.5 Hz with pulsation of 10–25% elongation of cells for 24–48 h ( n = 6). Reg3 γ was observed at 17 kDa, the values were normalized to β ‐actin (42 kDa, total protein fraction), and representative Western blots are shown. Gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001 treated cells versus control (ctrl) (One‐way ANOVA followed by a least significant difference post hoc test).$
Figure Legend Snippet: Regulation of regenerating islet‐derived 3 γ (Reg3 γ ) expression in cultured neonatal rat ventricular myocytes. Ventricular myocytes were exposed to lipopolysaccharide (LPS) (A, B) endothelin‐1 (ET‐1) (C) and fibroblast growth factor ‐1 (FGF‐1) (D) for 4–24 h ( n = 12–18). (E) Ventricular myocytes were exposed to cyclic mechanical stretch, in which the frequency of stretching was 0.5 Hz with pulsation of 10–25% elongation of cells for 24–48 h ( n = 6). Reg3 γ was observed at 17 kDa, the values were normalized to β ‐actin (42 kDa, total protein fraction), and representative Western blots are shown. Gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001 treated cells versus control (ctrl) (One‐way ANOVA followed by a least significant difference post hoc test).

Techniques Used: Derivative Assay, Expressing, Cell Culture, Western Blot, Gene Expression, Quantitative RT-PCR, Control

The effect of p38 MAPK inhibition on regenerating islet‐derived 3 γ (Reg3 γ ) mRNA levels in cardiac myocytes and in the heart in vivo. (A) Neonatal cardiac myocytes were treated with lipopolysaccharide (LPS) with and without SB203580 for 4 h ** P < 0.01, LPS versus control; ## P < 0.01, LPS + SB203580 versus LPS (One‐way ANOVA followed by a least significant difference post hoc test), n = 18. (B) The effect of p38 MAPK inhibition on mechanical stretch‐induced Reg3 γ gene expression in neonatal rat ventricular myocytes. Ventricular myocytes were exposed to cyclic mechanical stretch, in which the frequency of stretching was 0.5 Hz with pulsation of 10–25% elongation of cells for 24 h. *** P < 0.001, stretch versus control (one‐way ANOVA), n = 6. (C) Ang II was infused subcutaneously into rats with or without the p38 inhibitor SB203580 for 6 h. 0.9% NaCl was infused into control animals. White column, control; black column, Ang II; dark gray column, Ang II + SB203580; light gray column, SB203580. ** P < 0.01, Ang II versus control; and # P < 0.05, Ang II + SB203580 versus Ang II (one‐way ANOVA), n = 4–7. All gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 g mRNA to 18S mRNA, mean ± SEM.

Figure Legend Snippet: The effect of p38 MAPK inhibition on regenerating islet‐derived 3 γ (Reg3 γ ) mRNA levels in cardiac myocytes and in the heart in vivo. (A) Neonatal cardiac myocytes were treated with lipopolysaccharide (LPS) with and without SB203580 for 4 h ** P < 0.01, LPS versus control; ## P < 0.01, LPS + SB203580 versus LPS (One‐way ANOVA followed by a least significant difference post hoc test), n = 18. (B) The effect of p38 MAPK inhibition on mechanical stretch‐induced Reg3 γ gene expression in neonatal rat ventricular myocytes. Ventricular myocytes were exposed to cyclic mechanical stretch, in which the frequency of stretching was 0.5 Hz with pulsation of 10–25% elongation of cells for 24 h. *** P < 0.001, stretch versus control (one‐way ANOVA), n = 6. (C) Ang II was infused subcutaneously into rats with or without the p38 inhibitor SB203580 for 6 h. 0.9% NaCl was infused into control animals. White column, control; black column, Ang II; dark gray column, Ang II + SB203580; light gray column, SB203580. ** P < 0.01, Ang II versus control; and # P < 0.05, Ang II + SB203580 versus Ang II (one‐way ANOVA), n = 4–7. All gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 g mRNA to 18S mRNA, mean ± SEM.

Techniques Used: Inhibition, Derivative Assay, In Vivo, Control, Gene Expression, Quantitative RT-PCR

The effect of p38 MAPK overexpression on cardiac regenerating islet‐derived 3 γ (Reg3 γ ) mRNA levels in vitro and in vivo. (A) Reg3 γ mRNA levels from cultured NRCM transduced with recombinant adenoviruses overexpressing Mkk3bE and p38 α or control virus LacZ at the virus amounts of 4 MOI (2 + 2 MOI in combination). (B) Left ventricular Reg3 γ mRNA levels 3 days after Mkk3bE and p38 α gene transfer into left ventricle in rats compared to LacZ ‐injected hearts. White columns, control; black columns, p38 α MAPK + Mkk3bE. Gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 10–18). * P < 0.05, *** P < 0.001 p38 α + Mkk3bE versus control (Student's t ‐test). The immunohistochemical staining of Reg3 γ in the p38 α + Mkk3bE‐treated hearts. (C, E) LacZ indicates LacZ‐injected group and (D, F) p38MAPK group treated with p38 α and Mkk3bE viruses. The time point was 3 days. Magnification 10× (A, C), 40× (B, D). Scale bar 200 nmol L −1 (A, B), 50 nmol L −1 (C, D).

Figure Legend Snippet: The effect of p38 MAPK overexpression on cardiac regenerating islet‐derived 3 γ (Reg3 γ ) mRNA levels in vitro and in vivo. (A) Reg3 γ mRNA levels from cultured NRCM transduced with recombinant adenoviruses overexpressing Mkk3bE and p38 α or control virus LacZ at the virus amounts of 4 MOI (2 + 2 MOI in combination). (B) Left ventricular Reg3 γ mRNA levels 3 days after Mkk3bE and p38 α gene transfer into left ventricle in rats compared to LacZ ‐injected hearts. White columns, control; black columns, p38 α MAPK + Mkk3bE. Gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 10–18). * P < 0.05, *** P < 0.001 p38 α + Mkk3bE versus control (Student's t ‐test). The immunohistochemical staining of Reg3 γ in the p38 α + Mkk3bE‐treated hearts. (C, E) LacZ indicates LacZ‐injected group and (D, F) p38MAPK group treated with p38 α and Mkk3bE viruses. The time point was 3 days. Magnification 10× (A, C), 40× (B, D). Scale bar 200 nmol L −1 (A, B), 50 nmol L −1 (C, D).

Techniques Used: Over Expression, Derivative Assay, In Vitro, In Vivo, Cell Culture, Transduction, Recombinant, Control, Virus, Injection, Gene Expression, Quantitative RT-PCR, Immunohistochemical staining, Staining

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Journal: Physiological Reports

Article Title: Mitogen‐activated protein kinase p38 target regenerating islet‐derived 3 γ expression is upregulated in cardiac inflammatory response in the rat heart

doi: 10.14814/phy2.12996

Figure Lengend Snippet: Cardiac regenerating islet‐derived 3 γ (Reg3 γ ) gene expression in hypertrophied hearts and after myocardial infarction. Left ventricular Reg3 γ gene expression in spontaneously hypertensive rats (SHR) and in their age‐matched controls Wistar Kyoto rats (WKY). (A) White columns, WKY; black columns, SHR. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 4–11). *** P < 0.001 20‐month‐old SHR versus age‐matched WKY rats (Student's t ‐test). The effect of myocardial infarction (MI) on left ventricular Reg3 γ mRNA (B) and protein (C) levels in rats after 1 day and 2 weeks after MI. Reg3 γ was observed at 17 kDa, the values were normalized to GAPDH (36 kDa, total protein fraction), representative Western blots are shown. The controls went through the same invasive operation without the ligation of left anterior descending coronary artery. White columns, control; black columns, myocardial infarction. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA and total protein levels were assessed by Western blot analyses. Results are expressed as mean ± SEM ( n = 5–8). *** P < 0.001, ** P < 0.01, infarct versus control (Student's t ‐test).

Article Snippet: Antibody against rat Reg3 γ was produced in rabbits by GenScript Corporation (Piscataway, NJ).

Techniques: Derivative Assay, Gene Expression, Northern Blot, Western Blot, Ligation, Control

Journal: Physiological Reports

Article Title: Mitogen‐activated protein kinase p38 target regenerating islet‐derived 3 γ expression is upregulated in cardiac inflammatory response in the rat heart

doi: 10.14814/phy2.12996

Figure Lengend Snippet: Angiotensin II (Ang II) regulates cardiac regenerating islet‐derived 3 γ (Reg3 γ ) gene expression. The effect of subcutaneous administration of Ang II via osmotic minipumps for 6, 12, and 72 h, and 2 weeks on left ventricular Reg3 γ mRNA levels (A). White columns, control; black columns, Ang II. (B) The effect of subcutaneous administration of Ang II, losartan (Los) and their combination for 6 h on left ventricular Reg3 γ mRNA levels. White columns, control (ctrl); black columns, Ang II; dark gray column, Ang II + Los; light gray column, Los. Gene expression results measured by Northern Blot analysis are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 6–9). * P < 0.05, ** P < 0.01, *** P < 0.001, Ang II versus control (ctrl), ## P < 0.01 Ang II + losartan versus Ang II (One‐way ANOVA followed by a least significant difference post hoc test). Representative images demonstrating cardiac Reg3 γ (C, D) and alpha smooth muscle actin ( α ‐SMA) (E, F) expression in rats after 6 h‐infusion of Ang II. Control (ctrl) (C, E); Ang II (D, F). Magnification 100×, scale bar 100 μ mol L −1 .

Article Snippet: Antibody against rat Reg3 γ was produced in rabbits by GenScript Corporation (Piscataway, NJ).

Techniques: Derivative Assay, Gene Expression, Control, Northern Blot, Expressing

Journal: Physiological Reports

Article Title: Mitogen‐activated protein kinase p38 target regenerating islet‐derived 3 γ expression is upregulated in cardiac inflammatory response in the rat heart

doi: 10.14814/phy2.12996

Figure Lengend Snippet: Regulation of regenerating islet‐derived 3 γ (Reg3 γ ) expression in cultured neonatal rat ventricular myocytes. Ventricular myocytes were exposed to lipopolysaccharide (LPS) (A, B) endothelin‐1 (ET‐1) (C) and fibroblast growth factor ‐1 (FGF‐1) (D) for 4–24 h ( n = 12–18). (E) Ventricular myocytes were exposed to cyclic mechanical stretch, in which the frequency of stretching was 0.5 Hz with pulsation of 10–25% elongation of cells for 24–48 h ( n = 6). Reg3 γ was observed at 17 kDa, the values were normalized to β ‐actin (42 kDa, total protein fraction), and representative Western blots are shown. Gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001 treated cells versus control (ctrl) (One‐way ANOVA followed by a least significant difference post hoc test).

Article Snippet: Antibody against rat Reg3 γ was produced in rabbits by GenScript Corporation (Piscataway, NJ).

Techniques: Derivative Assay, Expressing, Cell Culture, Western Blot, Gene Expression, Quantitative RT-PCR, Control

Journal: Physiological Reports

Article Title: Mitogen‐activated protein kinase p38 target regenerating islet‐derived 3 γ expression is upregulated in cardiac inflammatory response in the rat heart

doi: 10.14814/phy2.12996

Figure Lengend Snippet: The effect of p38 MAPK inhibition on regenerating islet‐derived 3 γ (Reg3 γ ) mRNA levels in cardiac myocytes and in the heart in vivo. (A) Neonatal cardiac myocytes were treated with lipopolysaccharide (LPS) with and without SB203580 for 4 h ** P < 0.01, LPS versus control; ## P < 0.01, LPS + SB203580 versus LPS (One‐way ANOVA followed by a least significant difference post hoc test), n = 18. (B) The effect of p38 MAPK inhibition on mechanical stretch‐induced Reg3 γ gene expression in neonatal rat ventricular myocytes. Ventricular myocytes were exposed to cyclic mechanical stretch, in which the frequency of stretching was 0.5 Hz with pulsation of 10–25% elongation of cells for 24 h. *** P < 0.001, stretch versus control (one‐way ANOVA), n = 6. (C) Ang II was infused subcutaneously into rats with or without the p38 inhibitor SB203580 for 6 h. 0.9% NaCl was infused into control animals. White column, control; black column, Ang II; dark gray column, Ang II + SB203580; light gray column, SB203580. ** P < 0.01, Ang II versus control; and # P < 0.05, Ang II + SB203580 versus Ang II (one‐way ANOVA), n = 4–7. All gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 g mRNA to 18S mRNA, mean ± SEM.

Article Snippet: Antibody against rat Reg3 γ was produced in rabbits by GenScript Corporation (Piscataway, NJ).

Techniques: Inhibition, Derivative Assay, In Vivo, Control, Gene Expression, Quantitative RT-PCR

Journal: Physiological Reports

Article Title: Mitogen‐activated protein kinase p38 target regenerating islet‐derived 3 γ expression is upregulated in cardiac inflammatory response in the rat heart

doi: 10.14814/phy2.12996

Figure Lengend Snippet: The effect of p38 MAPK overexpression on cardiac regenerating islet‐derived 3 γ (Reg3 γ ) mRNA levels in vitro and in vivo. (A) Reg3 γ mRNA levels from cultured NRCM transduced with recombinant adenoviruses overexpressing Mkk3bE and p38 α or control virus LacZ at the virus amounts of 4 MOI (2 + 2 MOI in combination). (B) Left ventricular Reg3 γ mRNA levels 3 days after Mkk3bE and p38 α gene transfer into left ventricle in rats compared to LacZ ‐injected hearts. White columns, control; black columns, p38 α MAPK + Mkk3bE. Gene expression results measured by quantitative RT‐PCR are expressed as a ratio of Reg3 γ mRNA to 18S mRNA, mean ± SEM ( n = 10–18). * P < 0.05, *** P < 0.001 p38 α + Mkk3bE versus control (Student's t ‐test). The immunohistochemical staining of Reg3 γ in the p38 α + Mkk3bE‐treated hearts. (C, E) LacZ indicates LacZ‐injected group and (D, F) p38MAPK group treated with p38 α and Mkk3bE viruses. The time point was 3 days. Magnification 10× (A, C), 40× (B, D). Scale bar 200 nmol L −1 (A, B), 50 nmol L −1 (C, D).

Article Snippet: Antibody against rat Reg3 γ was produced in rabbits by GenScript Corporation (Piscataway, NJ).

Techniques: Over Expression, Derivative Assay, In Vitro, In Vivo, Cell Culture, Transduction, Recombinant, Control, Virus, Injection, Gene Expression, Quantitative RT-PCR, Immunohistochemical staining, Staining

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