Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway
Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereb...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Jin, Huiling [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
11 |
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| Übergeordnetes Werk: |
Enthalten in: Outcome of pregnancy in chronic myeloid leukaemia patients treated with tyrosine kinase inhibitors: Short report from a single centre - Alizadeh, H. ELSEVIER, 2015, New York, NY [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:108 ; year:2017 ; pages:170-180 ; extent:11 |
| Links: |
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| DOI / URN: |
10.1016/j.yjmcc.2017.05.014 |
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| 245 | 1 | 0 | |a Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway |
| 264 | 1 | |c 2017transfer abstract | |
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| 520 | |a Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. | ||
| 520 | |a Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. | ||
| 700 | 1 | |a Fujita, Takayuki |4 oth | |
| 700 | 1 | |a Jin, Meihua |4 oth | |
| 700 | 1 | |a Kurotani, Reiko |4 oth | |
| 700 | 1 | |a Namekata, Iyuki |4 oth | |
| 700 | 1 | |a Hamaguchi, Shogo |4 oth | |
| 700 | 1 | |a Hidaka, Yuko |4 oth | |
| 700 | 1 | |a Cai, Wenqian |4 oth | |
| 700 | 1 | |a Suita, Kenji |4 oth | |
| 700 | 1 | |a Ohnuki, Yoshiki |4 oth | |
| 700 | 1 | |a Mototani, Yasumasa |4 oth | |
| 700 | 1 | |a Shiozawa, Kouichi |4 oth | |
| 700 | 1 | |a Prajapati, Rajesh |4 oth | |
| 700 | 1 | |a Liang, Chen |4 oth | |
| 700 | 1 | |a Umemura, Masanari |4 oth | |
| 700 | 1 | |a Yokoyama, Utako |4 oth | |
| 700 | 1 | |a Sato, Motohiko |4 oth | |
| 700 | 1 | |a Tanaka, Hikaru |4 oth | |
| 700 | 1 | |a Okumura, Satoshi |4 oth | |
| 700 | 1 | |a Ishikawa, Yoshihiro |4 oth | |
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10.1016/j.yjmcc.2017.05.014 doi GBV00000000000269A.pica (DE-627)ELV040591794 (ELSEVIER)S0022-2828(17)30115-3 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Jin, Huiling verfasserin aut Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Fujita, Takayuki oth Jin, Meihua oth Kurotani, Reiko oth Namekata, Iyuki oth Hamaguchi, Shogo oth Hidaka, Yuko oth Cai, Wenqian oth Suita, Kenji oth Ohnuki, Yoshiki oth Mototani, Yasumasa oth Shiozawa, Kouichi oth Prajapati, Rajesh oth Liang, Chen oth Umemura, Masanari oth Yokoyama, Utako oth Sato, Motohiko oth Tanaka, Hikaru oth Okumura, Satoshi oth Ishikawa, Yoshihiro oth Enthalten in Elsevier Alizadeh, H. ELSEVIER Outcome of pregnancy in chronic myeloid leukaemia patients treated with tyrosine kinase inhibitors: Short report from a single centre 2015 New York, NY [u.a.] (DE-627)ELV012763152 volume:108 year:2017 pages:170-180 extent:11 https://doi.org/10.1016/j.yjmcc.2017.05.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 108 2017 170-180 11 045F 610 |
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10.1016/j.yjmcc.2017.05.014 doi GBV00000000000269A.pica (DE-627)ELV040591794 (ELSEVIER)S0022-2828(17)30115-3 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Jin, Huiling verfasserin aut Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Fujita, Takayuki oth Jin, Meihua oth Kurotani, Reiko oth Namekata, Iyuki oth Hamaguchi, Shogo oth Hidaka, Yuko oth Cai, Wenqian oth Suita, Kenji oth Ohnuki, Yoshiki oth Mototani, Yasumasa oth Shiozawa, Kouichi oth Prajapati, Rajesh oth Liang, Chen oth Umemura, Masanari oth Yokoyama, Utako oth Sato, Motohiko oth Tanaka, Hikaru oth Okumura, Satoshi oth Ishikawa, Yoshihiro oth Enthalten in Elsevier Alizadeh, H. ELSEVIER Outcome of pregnancy in chronic myeloid leukaemia patients treated with tyrosine kinase inhibitors: Short report from a single centre 2015 New York, NY [u.a.] (DE-627)ELV012763152 volume:108 year:2017 pages:170-180 extent:11 https://doi.org/10.1016/j.yjmcc.2017.05.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 108 2017 170-180 11 045F 610 |
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10.1016/j.yjmcc.2017.05.014 doi GBV00000000000269A.pica (DE-627)ELV040591794 (ELSEVIER)S0022-2828(17)30115-3 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Jin, Huiling verfasserin aut Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Fujita, Takayuki oth Jin, Meihua oth Kurotani, Reiko oth Namekata, Iyuki oth Hamaguchi, Shogo oth Hidaka, Yuko oth Cai, Wenqian oth Suita, Kenji oth Ohnuki, Yoshiki oth Mototani, Yasumasa oth Shiozawa, Kouichi oth Prajapati, Rajesh oth Liang, Chen oth Umemura, Masanari oth Yokoyama, Utako oth Sato, Motohiko oth Tanaka, Hikaru oth Okumura, Satoshi oth Ishikawa, Yoshihiro oth Enthalten in Elsevier Alizadeh, H. ELSEVIER Outcome of pregnancy in chronic myeloid leukaemia patients treated with tyrosine kinase inhibitors: Short report from a single centre 2015 New York, NY [u.a.] (DE-627)ELV012763152 volume:108 year:2017 pages:170-180 extent:11 https://doi.org/10.1016/j.yjmcc.2017.05.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 108 2017 170-180 11 045F 610 |
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10.1016/j.yjmcc.2017.05.014 doi GBV00000000000269A.pica (DE-627)ELV040591794 (ELSEVIER)S0022-2828(17)30115-3 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Jin, Huiling verfasserin aut Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Fujita, Takayuki oth Jin, Meihua oth Kurotani, Reiko oth Namekata, Iyuki oth Hamaguchi, Shogo oth Hidaka, Yuko oth Cai, Wenqian oth Suita, Kenji oth Ohnuki, Yoshiki oth Mototani, Yasumasa oth Shiozawa, Kouichi oth Prajapati, Rajesh oth Liang, Chen oth Umemura, Masanari oth Yokoyama, Utako oth Sato, Motohiko oth Tanaka, Hikaru oth Okumura, Satoshi oth Ishikawa, Yoshihiro oth Enthalten in Elsevier Alizadeh, H. ELSEVIER Outcome of pregnancy in chronic myeloid leukaemia patients treated with tyrosine kinase inhibitors: Short report from a single centre 2015 New York, NY [u.a.] (DE-627)ELV012763152 volume:108 year:2017 pages:170-180 extent:11 https://doi.org/10.1016/j.yjmcc.2017.05.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 108 2017 170-180 11 045F 610 |
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10.1016/j.yjmcc.2017.05.014 doi GBV00000000000269A.pica (DE-627)ELV040591794 (ELSEVIER)S0022-2828(17)30115-3 DE-627 ger DE-627 rakwb eng 610 610 DE-600 610 VZ 333.7 610 VZ 43.12 bkl 43.13 bkl 44.13 bkl Jin, Huiling verfasserin aut Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway 2017transfer abstract 11 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. Fujita, Takayuki oth Jin, Meihua oth Kurotani, Reiko oth Namekata, Iyuki oth Hamaguchi, Shogo oth Hidaka, Yuko oth Cai, Wenqian oth Suita, Kenji oth Ohnuki, Yoshiki oth Mototani, Yasumasa oth Shiozawa, Kouichi oth Prajapati, Rajesh oth Liang, Chen oth Umemura, Masanari oth Yokoyama, Utako oth Sato, Motohiko oth Tanaka, Hikaru oth Okumura, Satoshi oth Ishikawa, Yoshihiro oth Enthalten in Elsevier Alizadeh, H. ELSEVIER Outcome of pregnancy in chronic myeloid leukaemia patients treated with tyrosine kinase inhibitors: Short report from a single centre 2015 New York, NY [u.a.] (DE-627)ELV012763152 volume:108 year:2017 pages:170-180 extent:11 https://doi.org/10.1016/j.yjmcc.2017.05.014 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA SSG-OPC-GGO 43.12 Umweltchemie VZ 43.13 Umwelttoxikologie VZ 44.13 Medizinische Ökologie VZ AR 108 2017 170-180 11 045F 610 |
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Enthalten in Outcome of pregnancy in chronic myeloid leukaemia patients treated with tyrosine kinase inhibitors: Short report from a single centre New York, NY [u.a.] volume:108 year:2017 pages:170-180 extent:11 |
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Jin, Huiling @@aut@@ Fujita, Takayuki @@oth@@ Jin, Meihua @@oth@@ Kurotani, Reiko @@oth@@ Namekata, Iyuki @@oth@@ Hamaguchi, Shogo @@oth@@ Hidaka, Yuko @@oth@@ Cai, Wenqian @@oth@@ Suita, Kenji @@oth@@ Ohnuki, Yoshiki @@oth@@ Mototani, Yasumasa @@oth@@ Shiozawa, Kouichi @@oth@@ Prajapati, Rajesh @@oth@@ Liang, Chen @@oth@@ Umemura, Masanari @@oth@@ Yokoyama, Utako @@oth@@ Sato, Motohiko @@oth@@ Tanaka, Hikaru @@oth@@ Okumura, Satoshi @@oth@@ Ishikawa, Yoshihiro @@oth@@ |
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cardiac overexpression of epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits jak-stat pathway |
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Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway |
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Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. |
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Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. |
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Pro-inflammatory cytokines are released in septic shock and impair cardiac function via the Jak-STAT pathway. It is well known that sympathetic stimulation leads to coupling of the β-adrenergic receptor/Gs/adenylyl cyclase, a membrane-bound enzyme that catalyzes the conversion of ATP to cAMP, thereby stimulating protein kinase A (PKA) and ultimately compensating for cardiac dysfunction. The mechanism of such compensation by catecholamine has been traditionally understood as PKA-mediated enforcement of cardiac contractility. We hypothesized that exchange protein activated by cyclic AMP (Epac), a new target of cAMP signaling that functions independently of protein kinase A, also plays a key role in protection against acute stresses or changes in hemodynamic overload. |
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