Signaling via GPR30 protects the myocardium from ischemia/reperfusion injury

Brent R. Weil, Mariuxi C. Manukyan, Jeremy L. Herrmann, Yue Wang, Aaron M. Abarbanell, Jeffrey A. Poynter, Daniel R. Meldrum

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Abstract

Background: Estrogen may protect against the development of cardiovascular disease. Recently, a receptor known as GPR30 that seems to mediate estrogen's nongenomic effects has been identified. We hypothesized that the activation of GPR30 protects cardiac function and decreases myocardial inflammation after global ischemia/reperfusion (I/R). Methods: Hearts from male Sprague-Dawley rats were perfused via Langendorff and treated with either (1) vehicle; (2) 10 nm of the GPR30 agonist, G-1; or (3) 100 nm of G-1; they then were subjected to 25 minutes of ischemia and 40 minutes of reperfusion. Cardiac functional parameters were measured continuously. Ventricular tissue was analyzed for tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Results: At end-reperfusion, the left ventricular developed pressure in the 100-nm G-1 group was improved compared with vehicle (26% ± 12% equilibrium vs 54% ± 9% equilibrium; P < .05). Similar findings were noted when comparing the 100-nm G-1 group with the vehicle in terms of +dP/dt (53% ± 12% equilibrium vs 26% ± 19%, respectively; P < .05) and -dP/dt (56% ± 15% equilibrium vs 22% ± 16% equilibrium, respectively; P < .05). TNF-α, IL-1β, and IL-6 levels were lower in myocardium of the 100-nm G-1 group compared with the vehicle (P < .05). Conclusion: The GPR30 agonist, G-1, improves functional recovery and decreases myocardial inflammation after global I/R. GPR30 may play an important role in estrogen's ability to protect the heart against I/R injury.

Original languageEnglish
Pages (from-to)436-443
Number of pages8
JournalSurgery
Volume148
Issue number2
DOIs
StatePublished - 2010

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Reperfusion Injury
Reperfusion
Myocardium
Estrogens
Interleukin-1
Interleukin-6
Ischemia
Tumor Necrosis Factor-alpha
Inflammation
Ventricular Pressure
Sprague Dawley Rats
Cardiovascular Diseases

ASJC Scopus subject areas

  • Surgery

Cite this

Weil, B. R., Manukyan, M. C., Herrmann, J. L., Wang, Y., Abarbanell, A. M., Poynter, J. A., & Meldrum, D. R. (2010). Signaling via GPR30 protects the myocardium from ischemia/reperfusion injury. Surgery, 148(2), 436-443. https://doi.org/10.1016/j.surg.2010.03.011

Signaling via GPR30 protects the myocardium from ischemia/reperfusion injury. / Weil, Brent R.; Manukyan, Mariuxi C.; Herrmann, Jeremy L.; Wang, Yue; Abarbanell, Aaron M.; Poynter, Jeffrey A.; Meldrum, Daniel R.

In: Surgery, Vol. 148, No. 2, 2010, p. 436-443.

Research output: Contribution to journalArticle

Weil, BR, Manukyan, MC, Herrmann, JL, Wang, Y, Abarbanell, AM, Poynter, JA & Meldrum, DR 2010, 'Signaling via GPR30 protects the myocardium from ischemia/reperfusion injury', Surgery, vol. 148, no. 2, pp. 436-443. https://doi.org/10.1016/j.surg.2010.03.011
Weil BR, Manukyan MC, Herrmann JL, Wang Y, Abarbanell AM, Poynter JA et al. Signaling via GPR30 protects the myocardium from ischemia/reperfusion injury. Surgery. 2010;148(2):436-443. https://doi.org/10.1016/j.surg.2010.03.011
Weil, Brent R. ; Manukyan, Mariuxi C. ; Herrmann, Jeremy L. ; Wang, Yue ; Abarbanell, Aaron M. ; Poynter, Jeffrey A. ; Meldrum, Daniel R. / Signaling via GPR30 protects the myocardium from ischemia/reperfusion injury. In: Surgery. 2010 ; Vol. 148, No. 2. pp. 436-443.
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abstract = "Background: Estrogen may protect against the development of cardiovascular disease. Recently, a receptor known as GPR30 that seems to mediate estrogen's nongenomic effects has been identified. We hypothesized that the activation of GPR30 protects cardiac function and decreases myocardial inflammation after global ischemia/reperfusion (I/R). Methods: Hearts from male Sprague-Dawley rats were perfused via Langendorff and treated with either (1) vehicle; (2) 10 nm of the GPR30 agonist, G-1; or (3) 100 nm of G-1; they then were subjected to 25 minutes of ischemia and 40 minutes of reperfusion. Cardiac functional parameters were measured continuously. Ventricular tissue was analyzed for tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Results: At end-reperfusion, the left ventricular developed pressure in the 100-nm G-1 group was improved compared with vehicle (26{\%} ± 12{\%} equilibrium vs 54{\%} ± 9{\%} equilibrium; P < .05). Similar findings were noted when comparing the 100-nm G-1 group with the vehicle in terms of +dP/dt (53{\%} ± 12{\%} equilibrium vs 26{\%} ± 19{\%}, respectively; P < .05) and -dP/dt (56{\%} ± 15{\%} equilibrium vs 22{\%} ± 16{\%} equilibrium, respectively; P < .05). TNF-α, IL-1β, and IL-6 levels were lower in myocardium of the 100-nm G-1 group compared with the vehicle (P < .05). Conclusion: The GPR30 agonist, G-1, improves functional recovery and decreases myocardial inflammation after global I/R. GPR30 may play an important role in estrogen's ability to protect the heart against I/R injury.",
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AU - Weil, Brent R.

AU - Manukyan, Mariuxi C.

AU - Herrmann, Jeremy L.

AU - Wang, Yue

AU - Abarbanell, Aaron M.

AU - Poynter, Jeffrey A.

AU - Meldrum, Daniel R.

PY - 2010

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N2 - Background: Estrogen may protect against the development of cardiovascular disease. Recently, a receptor known as GPR30 that seems to mediate estrogen's nongenomic effects has been identified. We hypothesized that the activation of GPR30 protects cardiac function and decreases myocardial inflammation after global ischemia/reperfusion (I/R). Methods: Hearts from male Sprague-Dawley rats were perfused via Langendorff and treated with either (1) vehicle; (2) 10 nm of the GPR30 agonist, G-1; or (3) 100 nm of G-1; they then were subjected to 25 minutes of ischemia and 40 minutes of reperfusion. Cardiac functional parameters were measured continuously. Ventricular tissue was analyzed for tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Results: At end-reperfusion, the left ventricular developed pressure in the 100-nm G-1 group was improved compared with vehicle (26% ± 12% equilibrium vs 54% ± 9% equilibrium; P < .05). Similar findings were noted when comparing the 100-nm G-1 group with the vehicle in terms of +dP/dt (53% ± 12% equilibrium vs 26% ± 19%, respectively; P < .05) and -dP/dt (56% ± 15% equilibrium vs 22% ± 16% equilibrium, respectively; P < .05). TNF-α, IL-1β, and IL-6 levels were lower in myocardium of the 100-nm G-1 group compared with the vehicle (P < .05). Conclusion: The GPR30 agonist, G-1, improves functional recovery and decreases myocardial inflammation after global I/R. GPR30 may play an important role in estrogen's ability to protect the heart against I/R injury.

AB - Background: Estrogen may protect against the development of cardiovascular disease. Recently, a receptor known as GPR30 that seems to mediate estrogen's nongenomic effects has been identified. We hypothesized that the activation of GPR30 protects cardiac function and decreases myocardial inflammation after global ischemia/reperfusion (I/R). Methods: Hearts from male Sprague-Dawley rats were perfused via Langendorff and treated with either (1) vehicle; (2) 10 nm of the GPR30 agonist, G-1; or (3) 100 nm of G-1; they then were subjected to 25 minutes of ischemia and 40 minutes of reperfusion. Cardiac functional parameters were measured continuously. Ventricular tissue was analyzed for tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6. Results: At end-reperfusion, the left ventricular developed pressure in the 100-nm G-1 group was improved compared with vehicle (26% ± 12% equilibrium vs 54% ± 9% equilibrium; P < .05). Similar findings were noted when comparing the 100-nm G-1 group with the vehicle in terms of +dP/dt (53% ± 12% equilibrium vs 26% ± 19%, respectively; P < .05) and -dP/dt (56% ± 15% equilibrium vs 22% ± 16% equilibrium, respectively; P < .05). TNF-α, IL-1β, and IL-6 levels were lower in myocardium of the 100-nm G-1 group compared with the vehicle (P < .05). Conclusion: The GPR30 agonist, G-1, improves functional recovery and decreases myocardial inflammation after global I/R. GPR30 may play an important role in estrogen's ability to protect the heart against I/R injury.

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