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Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling

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Abstract

Catestatin (CST) is a catecholamine release-inhibitory peptide secreted from the adrenergic neurons and the adrenal glands. It regulates the cardiovascular functions and it is associated with cardiovascular diseases. Though its mechanisms of actions are not known, there are evidences of cross-talk between the adrenergic and CST signaling. We hypothesized that CST moderates the adrenergic overdrive and studied its effects on norepinephrine-mediated hypertrophic responses in H9c2 cardiac myoblasts. CST alone regulated the expression of a number of fetal genes that are induced during hypertrophy. When cells were pre-treated CST, it blunted the modulation of those genes by norepinephrine. Norepinephrine (2 µM) treatment also increased cell size and enhanced the level of Troponin T in the sarcomere. These effects were attenuated by the treatment with CST. CST attenuated the immediate generation of ROS and the increase in glutathione peroxidase activity induced by norepinephrine treatment. Expression of fosB and AP-1 promoter–reporter constructs was used as the endpoint readout for the interaction between the CST and adrenergic signals at the gene level. It showed that CST largely attenuates the stimulatory effects of norepinephrine and other mitogenic signals through the modulation of the gene regulatory modules in a characteristic manner. Depending upon the dose, the signaling by CST appears to be disparate, and at 10–25 nM doses, it primarily moderated the signaling by the β1/2-adrenoceptors. This study, for the first time, provides insights into the modulation of adrenergic signaling in the heart by CST.

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Abbreviations

Acta1:

Actin, alpha 1

AP-1:

Activator protein 1

ANP:

Atrial natriuretic peptide

AR:

Adrenergic receptor

cAMP:

Cyclic adenosine monophosphate

CEBP:

CCAAT/enhancer binding protein

cGMP:

Cyclic guanosine monophosphate

CHGA:

Chromogranin A

CST:

Catestatin

DCFH-DA:

Dichloro-dihydro-fluorescein diacetate

DHE:

Dihydroethidium

eNOS:

Endothelial nitric oxide synthase

FosB:

FBJ osteosarcoma oncogene B

GPx:

Glutathione peroxidase

HPF:

Hydroxyphenylfluorescein

ISO:

Isoproterenol

MAP:

Mitogen-activated protein

MHC:

Myosin heavy chain

PDE2:

Phosphodiesterase 2

PI3-kinase:

Phosphoinositide 3-kinase

PKA:

Protein kinase A

ROS:

Reactive oxygen species

SOD:

Superoxide dismutase

SP-1:

Specificity protein 1

References

  1. Fothergill LJ, Callaghan B, Hunne B et al (2017) Costorage of enteroendocrine hormones evaluated at the cell and subcellular levels in male mice. Endocrinology 158:2113–2123. https://doi.org/10.1210/en.2017-00243

    Article  CAS  PubMed  Google Scholar 

  2. Troger J, Theurl M, Kirchmair R et al (2017) Granin-derived peptides. Prog Neurobiol 154:37–61. https://doi.org/10.1016/j.pneurobio.2017.04.003

    Article  CAS  PubMed  Google Scholar 

  3. Bandyopadhyay GK, Mahata SK (2017) Chromogranin A regulation of obesity and peripheral insulin sensitivity. Front Endocrinol Lausanne 8:20. https://doi.org/10.3389/fendo.2017.00020

    Article  PubMed  PubMed Central  Google Scholar 

  4. Helle KB, Corti A (2015) Chromogranin A: a paradoxical player in angiogenesis and vascular biology. Cell Mol Life Sci CMLS 72:339–348. https://doi.org/10.1007/s00018-014-1750-9

    Article  CAS  PubMed  Google Scholar 

  5. Tota B, Angelone T, Cerra MC (2014) The surging role of Chromogranin A in cardiovascular homeostasis. Front Chem 2:64. https://doi.org/10.3389/fchem.2014.00064

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  6. Helle KB, Metz-Boutigue M-H, Cerra MC, Angelone T (2018) Chromogranins: from discovery to current times. Pflug Arch 470:143–154. https://doi.org/10.1007/s00424-017-2027-6

    Article  CAS  Google Scholar 

  7. Goetze JP, Alehagen U, Flyvbjerg A, Rehfeld JF (2014) Chromogranin A as a biomarker in cardiovascular disease. Biomark Med 8:133–140. https://doi.org/10.2217/bmm.13.102

    Article  CAS  PubMed  Google Scholar 

  8. Goetze JP, Hilsted LM, Rehfeld JF, Alehagen U (2014) Plasma chromogranin A is a marker of death in elderly patients presenting with symptoms of heart failure. Endocr Connect 3:47–56. https://doi.org/10.1530/EC-14-0017

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Gayen JR, Gu Y, O’Connor DT, Mahata SK (2009) Global disturbances in autonomic function yield cardiovascular instability and hypertension in the chromogranin a null mouse. Endocrinology 150:5027–5035. https://doi.org/10.1210/en.2009-0429

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Vaingankar SM, Li Y, Biswas N et al (2010) Effects of chromogranin A deficiency and excess in vivo: biphasic blood pressure and catecholamine responses. J Hypertens 28:817–825. https://doi.org/10.1097/HJH.0b013e328336ed3e

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Borges R, Dominguez N, Smith CB et al (2013) Granins and catecholamines: functional interaction in chromaffin cells and adipose tissue. Adv Pharmacol 68:93–113. https://doi.org/10.1016/B978-0-12-411512-5.00005-1

    Article  CAS  PubMed  Google Scholar 

  12. Loh YP, Cheng Y, Mahata SK et al (2012) Chromogranin A and derived peptides in health and disease. J Mol Neurosci MN 48:347–356. https://doi.org/10.1007/s12031-012-9728-2

    Article  CAS  PubMed  Google Scholar 

  13. Mahata SK, Kiranmayi M, Mahapatra NR (2017) Catestain: a master regulator of cardiovascular functions. Curr Med Chem. https://doi.org/10.2174/0929867324666170425100416

    Article  Google Scholar 

  14. Montesinos MS, Machado JD, Camacho M et al (2008) The crucial role of chromogranins in storage and exocytosis revealed using chromaffin cells from CHROMOGRANIN A null mouse. J Neurosci 28:3350–3358. https://doi.org/10.1523/JNEUROSCI.5292-07.2008

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  15. Bandyopadhyay GK, Vu CU, Gentile S et al (2012) Catestatin (chromogranin A(352–372)) and novel effects on mobilization of fat from adipose tissue through regulation of adrenergic and leptin signaling. J Biol Chem 287:23141–23151. https://doi.org/10.1074/jbc.M111.335877

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Wang D, Liu T, Shi S et al (2016) Chronic administration of catestatin improves autonomic function and exerts cardioprotective effects in myocardial infarction rats. J Cardiovasc Pharmacol Ther 21:526–535. https://doi.org/10.1177/1074248416628676

    Article  CAS  PubMed  Google Scholar 

  17. Wu Z, Zhu D (2014) The important role of catestatin in cardiac remodeling. Biomark Biochem Indic Expo Response Susceptibility Chem 19:625–630. https://doi.org/10.3109/1354750X.2014.950331

    Article  CAS  Google Scholar 

  18. Angelone T, Quintieri AM, Pasqua T et al (2015) The NO stimulator, Catestatin, improves the Frank–Starling response in normotensive and hypertensive rat hearts. Nitric Oxide 50:10–19. https://doi.org/10.1016/j.niox.2015.07.004

    Article  CAS  PubMed  Google Scholar 

  19. Fung MM, Salem RM, Mehtani P et al (2010) Direct vasoactive effects of the chromogranin A (CHGA) peptide catestatin in humans in vivo. Clin Exp Hypertens 32:278–287. https://doi.org/10.3109/10641960903265246

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  20. Theurl M, Schgoer W, Albrecht K et al (2010) The neuropeptide catestatin acts as a novel angiogenic cytokine via a basic fibroblast growth factor-dependent mechanism. Circ Res 107:1326–1335. https://doi.org/10.1161/CIRCRESAHA.110.219493

    Article  CAS  PubMed  Google Scholar 

  21. Zhu D, Xie H, Wang X et al (2017) Catestatin-A novel predictor of left ventricular remodeling after acute myocardial infarction. Sci Rep. https://doi.org/10.1038/srep44168

    Article  PubMed  PubMed Central  Google Scholar 

  22. de Lucia C, Femminella GD, Gambino G et al (2014) Adrenal adrenoceptors in heart failure. Front Physiol 5:246. https://doi.org/10.3389/fphys.2014.00246

    Article  PubMed  PubMed Central  Google Scholar 

  23. Jensen BC, O’Connell TD, Simpson PC (2011) Alpha-1-adrenergic receptors: targets for agonist drugs to treat heart failure. J Mol Cell Cardiol 51:518–528. https://doi.org/10.1016/j.yjmcc.2010.11.014

    Article  CAS  PubMed  Google Scholar 

  24. Lymperopoulos A (2013) Physiology and pharmacology of the cardiovascular adrenergic system. Front Physiol 4:240. https://doi.org/10.3389/fphys.2013.00240

    Article  PubMed  PubMed Central  Google Scholar 

  25. Pérez-Schindler J, Philp A, Hernandez-Cascales J (2013) Pathophysiological relevance of the cardiac β2-adrenergic receptor and its potential as a therapeutic target to improve cardiac function. Eur J Pharmacol 698:39–47. https://doi.org/10.1016/j.ejphar.2012.11.001

    Article  CAS  PubMed  Google Scholar 

  26. Weber S, Meyer-Roxlau S, El-Armouche A (2016) Role of protein phosphatase inhibitor-1 in cardiac beta adrenergic pathway. J Mol Cell Cardiol 101:116–126. https://doi.org/10.1016/j.yjmcc.2016.09.007

    Article  CAS  PubMed  Google Scholar 

  27. Gaede AH, Pilowsky PM (2012) Catestatin, a chromogranin A-derived peptide, is sympathoinhibitory and attenuates sympathetic barosensitivity and the chemoreflex in rat CVLM. Am J Physiol Regul Integr Comp Physiol 302:R365–R372. https://doi.org/10.1152/ajpregu.00409.2011

    Article  CAS  PubMed  Google Scholar 

  28. Mazza R, Tota B, Gattuso A (2015) Cardio-vascular activity of catestatin: interlocking the puzzle pieces. Curr Med Chem 22:292–304

    Article  CAS  Google Scholar 

  29. Angelone T, Quintieri AM, Brar BK et al (2008) The antihypertensive chromogranin a peptide catestatin acts as a novel endocrine/paracrine modulator of cardiac inotropism and lusitropism. Endocrinology 149:4780–4793. https://doi.org/10.1210/en.2008-0318

    Article  PubMed  PubMed Central  Google Scholar 

  30. Angelone T, Quintieri AM, Pasqua T et al (2012) Phosphodiesterase type-2 and NO-dependent S-nitrosylation mediate the cardioinhibition of the antihypertensive catestatin. Am J Physiol Heart Circ Physiol 302:H431–H442. https://doi.org/10.1152/ajpheart.00491.2011

    Article  CAS  PubMed  Google Scholar 

  31. Rodrigues JV, Gomes CM (2010) Enhanced superoxide and hydrogen peroxide detection in biological assays. Free Radic Biol Med 49:61–66. https://doi.org/10.1016/j.freeradbiomed.2010.03.014

    Article  CAS  PubMed  Google Scholar 

  32. Weydert CJ, Cullen JJ (2010) Measurement of superoxide dismutase, catalase and glutathione peroxidase in cultured cells and tissue. Nat Protoc 5:51–66. https://doi.org/10.1038/nprot.2009.197

    Article  CAS  PubMed  Google Scholar 

  33. Marklund S, Marklund G (1974) Involvement of the superoxide anion radical in the autoxidation of pyrogallol and a convenient assay for superoxide dismutase. Eur J Biochem FEBS 47:469–474

    Article  CAS  Google Scholar 

  34. Gupta MK, Neelakantan TV, Sanghamitra M et al (2006) An assessment of the role of reactive oxygen species and redox signaling in norepinephrine-induced apoptosis and hypertrophy of H9c2 cardiac myoblasts. Antioxid Redox Signal 8:1081–1093. https://doi.org/10.1089/ars.2006.8.1081

    Article  CAS  PubMed  Google Scholar 

  35. Saleem N, Goswami SK (2017) Activation of adrenergic receptor in H9c2 cardiac myoblasts co-stimulates Nox2 and the derived ROS mediate the downstream responses. Mol Cell Biochem. https://doi.org/10.1007/s11010-017-3088-8

    Article  PubMed  Google Scholar 

  36. Bassino E, Fornero S, Gallo MP et al (2015) Catestatin exerts direct protective effects on rat cardiomyocytes undergoing ischemia/reperfusion by stimulating PI3K-Akt-GSK3β pathway and preserving mitochondrial membrane potential. PLoS ONE. https://doi.org/10.1371/journal.pone.0119790

    Article  PubMed  PubMed Central  Google Scholar 

  37. Liao F, Zheng Y, Cai J et al (2015) Catestatin attenuates endoplasmic reticulum induced cell apoptosis by activation type 2 muscarinic acetylcholine receptor in cardiac ischemia/reperfusion. Sci Rep. https://doi.org/10.1038/srep16590

    Article  PubMed  PubMed Central  Google Scholar 

  38. Dirkx E, da Costa Martins PA, De Windt LJ (2013) Regulation of fetal gene expression in heart failure. Biochim Biophys Acta 1832:2414–2424. https://doi.org/10.1016/j.bbadis.2013.07.023

    Article  CAS  PubMed  Google Scholar 

  39. Kanaan GN, Harper ME (2017) Cellular redox dysfunction in the development of cardiovascular diseases. Biochim Biophys Acta. https://doi.org/10.1016/j.bbagen.2017.07.027

    Article  Google Scholar 

  40. Jindal E, Goswami SK (2011) In cardiac myoblasts, cellular redox regulates FosB and Fra-1 through multiple cis-regulatory modules. Free Radic Biol Med 51:1512–1521. https://doi.org/10.1016/j.freeradbiomed.2011.07.008

    Article  CAS  PubMed  Google Scholar 

  41. Saleem N, Prasad A, Goswami SK (2018) Apocynin prevents isoproterenol-induced cardiac hypertrophy in rat. Mol Cell Biochem 445:79–88. https://doi.org/10.1007/s11010-017-3253-0

    Article  CAS  PubMed  Google Scholar 

  42. Thakur A, Alam MJ, Ajayakumar MR et al (2015) Norepinephrine-induced apoptotic and hypertrophic responses in H9c2 cardiac myoblasts are characterized by different repertoire of reactive oxygen species generation. Redox Biol 5:243–252. https://doi.org/10.1016/j.redox.2015.05.005

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  43. Wang Y, Branicky R, Noë A, Hekimi S (2018) Superoxide dismutases: dual roles in controlling ROS damage and regulating ROS signaling. J Cell Biol 217:1915–1928. https://doi.org/10.1083/jcb.201708007

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  44. Cabassi A, Binno SM, Tedeschi S et al (2014) Low serum ferroxidase I activity is associated with mortality in heart failure and related to both peroxynitrite-induced cysteine oxidation and tyrosine nitration of ceruloplasmin. Circ Res 114:1723–1732. https://doi.org/10.1161/CIRCRESAHA.114.302849

    Article  CAS  PubMed  Google Scholar 

  45. Paulova H, Stracina T, Jarkovsky J et al (2013) Hydroxyl radicals’ production and ECG parameters during ischemia and reperfusion in rat, guinea pig and rabbit isolated heart. Gen Physiol Biophys 32:221–228. https://doi.org/10.4149/gpb_2013016

    Article  CAS  PubMed  Google Scholar 

  46. Sies H, Berndt C, Jones DP (2017) Oxidative Stress. Annu Rev Biochem 86:715–748. https://doi.org/10.1146/annurev-biochem-061516-045037

    Article  CAS  PubMed  Google Scholar 

  47. Barančík M, Grešová L, Barteková M, Dovinová I (2016) Nrf2 as a key player of redox regulation in cardiovascular diseases. Physiol Res 65(Suppl 1):S1–S10

    PubMed  Google Scholar 

  48. Gang C, Qiang C, Xiangli C et al (2015) Puerarin suppresses angiotensin II-induced cardiac hypertrophy by inhibiting NADPH oxidase activation and oxidative stress-triggered AP-1 signaling pathways. J Pharm Pharm Sci 18:235–248

    Article  Google Scholar 

  49. Hill C, Würfel A, Heger J et al (2013) Inhibition of AP-1 signaling by JDP2 overexpression protects cardiomyocytes against hypertrophy and apoptosis induction. Cardiovasc Res 99:121–128. https://doi.org/10.1093/cvr/cvt094

    Article  CAS  PubMed  Google Scholar 

  50. Suzuki T, Yamamoto M (2017) Stress-sensing mechanisms and the physiological roles of the Keap1-Nrf2 system during cellular stress. J Biol Chem. https://doi.org/10.1074/jbc.R117.800169

    Article  PubMed  PubMed Central  Google Scholar 

  51. Windak R, Müller J, Felley A et al (2013) The AP-1 transcription factor c-Jun prevents stress-imposed maladaptive remodeling of the heart. PLoS ONE 8:e73294. https://doi.org/10.1371/journal.pone.0073294

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  52. Selvaraj N, Budka JA, Ferris MW et al (2015) Extracellular signal-regulated kinase signaling regulates the opposing roles of JUN family transcription factors at ETS/AP-1 sites and in cell migration. Mol Cell Biol 35:88–100. https://doi.org/10.1128/MCB.00982-14

    Article  CAS  PubMed  Google Scholar 

  53. Li P, Spolski R, Liao W, Leonard WJ (2014) Complex interactions of transcription factors in mediating cytokine biology in T cells. Immunol Rev 261:141–156. https://doi.org/10.1111/imr.12199

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. Fujita T, Toya Y, Iwatsubo K et al (2001) Accumulation of molecules involved in alpha1-adrenergic signal within caveolae: caveolin expression and the development of cardiac hypertrophy. Cardiovasc Res 51:709–716

    Article  CAS  Google Scholar 

  55. Gesmundo I, Miragoli M, Carullo P et al (2017) Growth hormone-releasing hormone attenuates cardiac hypertrophy and improves heart function in pressure overload-induced heart failure. Proc Natl Acad Sci USA 114:12033–12038. https://doi.org/10.1073/pnas.1712612114

    Article  CAS  PubMed  Google Scholar 

  56. Ianoul A, Grant DD, Rouleau Y et al (2005) Imaging nanometer domains of beta-adrenergic receptor complexes on the surface of cardiac myocytes. Nat Chem Biol 1:196–202. https://doi.org/10.1038/nchembio726

    Article  CAS  PubMed  Google Scholar 

  57. Vyas FS, Nelson CP, Dickenson JM (2018) Role of transglutaminase 2 in A1 adenosine receptor- and β2-adrenoceptor-mediated pharmacological pre- and post-conditioning against hypoxia-reoxygenation-induced cell death in H9c2 cells. Eur J Pharmacol 819:144–160. https://doi.org/10.1016/j.ejphar.2017.11.049

    Article  CAS  PubMed  Google Scholar 

  58. Crowley LC, Marfell BJ, Scott AP et al (2016) Dead cert: measuring cell death. Cold Spring Harb Protoc. https://doi.org/10.1101/pdb.top070318

    Article  PubMed  Google Scholar 

  59. Barry SP, Davidson SM, Townsend PA (2008) Molecular regulation of cardiac hypertrophy. Int J Biochem Cell Biol 40:2023–2039. https://doi.org/10.1016/j.biocel.2008.02.020

    Article  CAS  PubMed  Google Scholar 

  60. Fu Y, Xiao H, Zhang Y (2012) Beta-adrenoceptor signaling pathways mediate cardiac pathological remodeling. Front Biosci Elite Ed 4:1625–1637

    Article  Google Scholar 

  61. O’Connell TD, Jensen BC, Baker AJ, Simpson PC (2014) Cardiac alpha1-adrenergic receptors: novel aspects of expression, signaling mechanisms, physiologic function, and clinical importance. Pharmacol Rev 66:308–333. https://doi.org/10.1124/pr.112.007203

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  62. Manda G, Isvoranu G, Comanescu MV et al (2015) The redox biology network in cancer pathophysiology and therapeutics. Redox Biol 5:347–357. https://doi.org/10.1016/j.redox.2015.06.014

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  63. Spencer NY, Engelhardt JF (2014) The basic biology of redoxosomes in cytokine-mediated signal transduction and implications for disease-specific therapies. Biochemistry 53:1551–1564. https://doi.org/10.1021/bi401719r

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  64. Sam F, Kerstetter DL, Pimental DR et al (2005) Increased reactive oxygen species production and functional alterations in antioxidant enzymes in human failing myocardium. J Card Fail 11:473–480. https://doi.org/10.1016/j.cardfail.2005.01.007

    Article  CAS  PubMed  Google Scholar 

  65. Srivastava S, Chandrasekar B, Gu Y et al (2007) Downregulation of CuZn-superoxide dismutase contributes to beta-adrenergic receptor-mediated oxidative stress in the heart. Cardiovasc Res 74:445–455. https://doi.org/10.1016/j.cardiores.2007.02.016

    Article  CAS  PubMed  Google Scholar 

  66. Kiranmayi M, Chirasani VR, Allu PKR et al (2016) Catestatin Gly364Ser variant alters systemic blood pressure and the risk for hypertension in human populations via endothelial nitric oxide pathway. Hypertens Dallas Tex 68:334–347. https://doi.org/10.1161/HYPERTENSIONAHA.116.06568

    Article  CAS  Google Scholar 

  67. Sahu BS, Mohan J, Obbineni JM et al (2012) Molecular interactions of the physiological anti-hypertensive peptide catestatin with the neuronal nicotinic acetylcholine receptor. J Cell Sci 125:2323–2337. https://doi.org/10.1242/jcs.103176

    Article  CAS  PubMed  Google Scholar 

  68. Schmidt SF, Madsen JG, Frafjord KO et al (2016) Integrative genomics outlines a biphasic glucose response and a ChREBP-RORgamma axis regulating proliferation in beta cells. Cell Rep 16:2359–2372. https://doi.org/10.1016/j.celrep.2016.07.063

    Article  CAS  PubMed  Google Scholar 

  69. Zhang X, Meng J, Wang ZY (2012) A switch role of Src in the biphasic EGF signaling of ER-negative breast cancer cells. PLoS ONE 7:e41613. https://doi.org/10.1371/journal.pone.0041613

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  70. Kazanietz MG, Gutkind JS, Puyo A et al (1989) Further evidence of interaction between vasodilator beta 2- and vasoconstrictor alpha 2-adrenoceptor-mediated responses in maintaining vascular tone in anesthetized rats. J Cardiovasc Pharmacol 14:874–880

    Article  CAS  Google Scholar 

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Acknowledgements

The authors thankfully acknowledge the funding supports from the Department of Biotechnology [DBT], Government of India (BT/PR4268/BRB/10/1016/2011 awarded to SKG; BT/PR12820/ BRB/10/726/2009 to NRM). Partial support also came from the DST-PURSE funding support to the Jawaharlal Nehru University. MJA is a recipient of JR/SR Fellowship from DBT, Government of India.

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  1. Md. Jahangir Alam

    Present address: Translational Health Science and Technology Institute, NCR Biotech Science Cluster, Fridabad, 121001, India

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  1. Translational Health Science and Technology Institute, NCR Biotech Science Cluster, Fridabad, 121001, India

    Shyamal K. Goswami

  2. School of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India

    Richa Gupta

  3. Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai, 600036, India

    Nitish R. Mahapatra

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Alam, M.J., Gupta, R., Mahapatra, N.R. et al. Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling. Mol Cell Biochem 464, 205–219 (2020). https://doi.org/10.1007/s11010-019-03661-1

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