Intermedin/adrenomedullin2: an autocrine/paracrine factor in vascular homeostasis and disease

Ni, Xian-Qiang; Zhang, Jinsheng; Tang, Chaoshu; Qi, Yongfen

doi:10.1007/s11427-014-4701-7

Cited by 33 publications

(29 citation statements)

References 38 publications

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“…Human IMD gene is located on the distal arm of chromosome 22, and its prepropeptide is composed of 148 amino acids, named prepro-IMD. Prepro-IMD can yield IMD 1–47 (prepro-IMD 101—147 ), IMD 8–47 (prepro-IMD 108–147 ), and IMD 1–53 (prepro-IMD 93–145 ) by proteolytic cleavage and amidation 26) . IMD has the similar effects with adrenomedullin.…”

Section: Introductionmentioning

confidence: 99%

“…Adrenomedullin receptor activity modifying protein (RAMP)2 system can maintain vascular integrity and homeostasis 27) . IMD can also maintain cardiovascular homeostasis via its calcitonin receptor-like receptor (CRLR)/RAMP complexes 26) . Our previous study showed that in CFs, endogenous IMD was significantly decreased in response to Ang II treatment, and administration of IMD 1–53 suppressed Ang II-induced activation of CFs and hypertrophy of cardiomyocytes 28, 29) .…”

Section: Introductionmentioning

confidence: 99%

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Intermedin<sub>1–53</sub> Protects Against Myocardial Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Inflammation Induced by Homocysteine in Apolipoprotein E-Deficient Mice

Zhang

Hou

et al. 2016

J Atheroscler Thromb

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Aim: Endoplasmic reticulum stress (ERS) and inflammation participate in cardiac fibrosis. Importantly, a novel paracrine/autocrine peptide intermedin1–53 (IMD1–53) in the heart inhibits myocardial fibrosis in rats. However, the mechanisms are yet to be fully elucidated.Methods: Myocardial fibrosis in apolipoprotein E-deficient (ApoE -/-) mice and neonatal rat cardiac fibroblasts (CFs) were induced using homocysteine (Hcy).Results: IMD1–53 inhibited myocardial fibrosis in vivo and in vitro. Picrosirius red staining showed that IMD1–53 reduced myocardial interstitial collagen deposition in ApoE-/- mice treated with Hcy and decreased the expression of myocardial collagen I and III, which was further verified in rat CFs. IMD1–53 attenuated myocardial hypertrophy, as shown by cardiomyocyte cross-sectional area, ratio of heart weight to body weight, and mRNA levels of atrial natriuretic peptide and brain natriuretic peptide. IMD1–53 inhibited the upregulation of ERS hallmarkers such as glucose-regulated protein 78 (GRP78), GRP94, activating transcription factor 6 (ATF6), ATF4, inositol-requiring enzyme 1α, spliced-X-box-binding protein-1, protein kinase receptor-like ER kinase, and eukaryotic translation initiation factor 2α in mouse myocardium and rat CFs treated with Hcy. In addition, IMD1–53 decreased the production of inflammatory factors such as tumor necrosis factor-α, monocyte chemotactic protein-1, interleukin-6 (IL-6), and IL-1β in the mouse myocardium and rat CFs treated with Hcy. Concurrently, IMD1–53 ameliorated the expression of nuclear factor-κB, transforming growth factor-β1, and c-Jun N-terminal kinase in the mouse myocardium and rat CFs treated with Hcy.Conclusions: IMD potentially protects against myocardial fibrosis induced by Hcy in ApoE-/- mice, possibly via attenuating myocardial ERS and inflammation.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Intermedin<sub>1–53</sub> Protects Against Myocardial Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Inflammation Induced by Homocysteine in Apolipoprotein E-Deficient Mice

Zhang

Hou

et al. 2016

J Atheroscler Thromb

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“…The symptoms of PH were alleviated with ADM2/IMD treatment in rats, the right ventricular hypertrophy was prevented and the hypoxic pulmonary vascular remodeling was inhibited 111 . According to these studies that were performed in pulmonary hypertensive rats, ADM2/IMD is thought to be effective in PH 118 . In chronic hypoxiainduced PH ADM2/IMD provided potent vasodilation in pulmonary arteries of rats and intraarterial administration was reduced the perfusion pressure of hypoxic lungs.…”

Section: U N C O R R E C T E D P R O O Fmentioning

confidence: 99%

The Cardiopulmonary Effects of Calcitonin-Gene Related Peptide Family

Telli¹,

Tel²,

Gümüşel³

2019

tjps

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The cardiopulmonary diseases are very common in the population. They are high-cost diseases and there are still no definitive treatments. The roles of members of the calcitonin-gene-related peptide (CGRP) family in the cardiopulmonary diseases have been studied for many years and promising results are obtained. Especially in recent years, two important members of the family, adrenomedullin and adrenomedullin2/intermedin, are considered as new treatment targets in cardiopulmonary diseases. In this review, the roles of CGRP family peptides in cardiopulmonary diseases has been investigated according to the studies that were performed to the present day.

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“…Intermedin (IMD), also named as adrenomedullin-2, a member of the calcitonin/calcitonin gene-related peptide (CGRP) family, exerts a wide range of biological effects, especially in maintaining cardiovascular homeostasis [8]. The possible mechanism may be related to the upregulation in cAMP level in the circulatory system, and regulation of the proliferation of the smooth muscle and up-regulating NO system [9].…”

Section: Introductionmentioning

confidence: 99%

Plasma Intermedin Level Indicates Severity and Treatment Efficacy of Septic Shock in Sprague-Dawley (SD) Rats

Yang

Chen

et al. 2016

Med Sci Monit

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BackgroundThe aim of this study was to investigate the value of plasma intermedin (IMD) in assessing severity and treatment efficacy of septic shock.Material/MethodsHealthy male Sprague-Dawley (SD) rats were chosen and divided into a normal control group (n=15) and a shock model group (n=27) that received intravenous injection of lipopolysaccharide (LPS). Then, 3 specimens were taken from each group. The shock model group rats were divided into an LPS group and a treatment group with 12 rats each. The treatment group received intravenous injection of compound sodium lactate solution. Plasma IMD and IMD1-47 mRNA expressions were compared and analyzed.ResultsMean arterial pressure (MAP) was lower while white blood cell count and TNF-α were higher in the shock model group than in the normal control group (P<0.05). After 10 h and 20 h, the treatment group had lower plasma IMD and IMD1-47 mRNA expressions compared with the LPS group (P<0.05). Plasma IMD and IMD1-47 mRNA expressions in the LPS group after 20 h were significantly higher than after 10 h (P<0.05). IMD was positively correlated with interleukins (IL-3, IL-6, and IL-8), white blood cell count, and body temperature (all P<0.05), but were negatively correlated with systolic pressure (r=−0.8474, P=0.0040).ConclusionsPlasma IMD level can effectively reflect the severity of septic shock and can be used as an important indicator of septic shock treatment effectiveness.

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Intermedin/adrenomedullin2: an autocrine/paracrine factor in vascular homeostasis and disease

Cited by 33 publications

References 38 publications

Intermedin<sub>1–53</sub> Protects Against Myocardial Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Inflammation Induced by Homocysteine in Apolipoprotein E-Deficient Mice

Intermedin<sub>1–53</sub> Protects Against Myocardial Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Inflammation Induced by Homocysteine in Apolipoprotein E-Deficient Mice

The Cardiopulmonary Effects of Calcitonin-Gene Related Peptide Family

Plasma Intermedin Level Indicates Severity and Treatment Efficacy of Septic Shock in Sprague-Dawley (SD) Rats

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