Matches in SemOpenAlex for { <https://semopenalex.org/work/W3202040765> ?p ?o ?g. }
Showing items 1 to 67 of
67
with 100 items per page.
- W3202040765 abstract "HomeCirculationVol. 144, No. 13Response by Zhao et al to Letter Regarding Article, “Role of IgE-FcεRI in Pathological Cardiac Remodeling and Dysfunction” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessLetterPDF/EPUBResponse by Zhao et al to Letter Regarding Article, “Role of IgE-FcεRI in Pathological Cardiac Remodeling and Dysfunction” Hongmei Zhao, PhD, Chi Geng, MSc, Chen Yan, PhD and Jing Wang, MD, PhD Hongmei ZhaoHongmei Zhao State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Department of Pathophysiology, Peking Union Medical College, Beijing (H.Z., C.GT., J.W.). Search for more papers by this author , Chi GengChi Geng https://orcid.org/0000-0002-9737-7271 State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Department of Pathophysiology, Peking Union Medical College, Beijing (H.Z., C.GT., J.W.). Search for more papers by this author , Chen YanChen Yan Aab Cardiovascular Research Institute, University of Rochester, School of Medicine and Dentistry, NY (C.Y.). Search for more papers by this author and Jing WangJing Wang https://orcid.org/0000-0003-2410-5408 State Key Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Department of Pathophysiology, Peking Union Medical College, Beijing (H.Z., C.GT., J.W.). Search for more papers by this author Originally published27 Sep 2021https://doi.org/10.1161/CIRCULATIONAHA.121.055680Circulation. 2021;144:e216–e217In Response:We appreciate Varricchi et al for their interest in our publication1 and their comments regarding the contribution of mast cells in immunoglobulin E (IgE)-FcεR1–mediated cardiac remodeling. Based on our in vitro and in vivo studies, we demonstrated that IgE-FcεR1 signaling contributes to cardiac remodeling and dysfunction induced by neurohormonal overactivation or pressure overload.1 IgE-FcεR1 is also important for cardiomyocyte hypertrophy and cardiac fibroblast (CF) activation.1 The role of CFs in cardiac remodeling/fibrosis has been further proved by our recent publication using CF-specific FcεR1-knockout mice.2We demonstrated that cultured cardiomyocytes and CFs express considerable levels of FcεR1, and that IgE directly promotes cardiomyocyte hypertrophy and CF activation in vitro.1 Varricchi et al raised a concern regarding mast cell contamination in these cardiomyocyte/CF studies. Our responses to this concern include the following: (1) Cardiac mast cells are almost absent at the birth of neonatal rats3 and remain very low up to 11 to 12 days (0.35±0.06 mast cells/mm2).4 We used neonatal rats at ≈3 days of age, suggesting extremely low levels of mast cells in these neonates. (2) Cardiomyocytes/CFs are adherent cells, whereas mast cells are nonadherent cells in primary culture. Any mast cells should be removed after several washing steps during cardiomyocyte/CF isolation/culture. (3) The methods used for cardiomyocyte/CF isolation are well established, which produce cells with >95% purity.2 Therefore, we believe that our observations in cultured cardiomyocytes/CFs are unlikely to have resulted from mast cell contamination.We performed a bone marrow (BM) transplantation study and demonstrated that FcεR1-mediated regulation of cardiac remodeling is independent of BM-derived cells. Varricchi et al raised a concern that mast cells in the BM of recipient mice may not be killed by gamma radiation because of mast cell resistance to radiation. It has been reported that mast cells present in different tissues exhibit distinct sensitivities to radiation. For example, as cited by Varricchi et al, mast cells in skin are resistant to 400 cGy radiation. However, it has also been reported that mast cell precursors in BM are sensitive to radiation.5 Thus, the high-dose x-ray (800 cGy) that we used should effectively remove BM-derived mast cells.Varricchi et al mentioned previous findings that omalizumab downregulates FcεR1 expression in human basophils and mast cells. This raises an interesting question regarding whether omalizumab also downregulates the expression of FcεR1 in cardiomyocytes/CFs, which remains to be determined. Nevertheless, our results showed that omalizumab blocked cardiac remodeling and improved cardiac function through blocking the IgE-FcεR1 signaling, regardless of targeting IgE, downregulating FcεR1, or both.The pathophysiological roles of cardiac mast cells remain controversial, which are either beneficial or detrimental depending on the type and stage of pathological status. We agree with Varricchi et al and do not exclude the possibility of mast cell contribution in IgE-induced cardiac remodeling. Findings from our studies strongly support the conclusion that the role of IgE-FcεR1 in cardiac remodeling and dysfunction is at least in part through the direct effects on cardiomyocytes and CFs. The role of mast cells in pathological cardiac remodeling deserves to be evaluated in the future with mast cell–specific FcεR1 knockout mice.Disclosures None.Footnoteshttps://www.ahajournals.org/journal/circReferences1. Zhao H, Yang H, Geng C, Chen Y, Pang J, Shu T, Zhao M, Tang Y, Li Z, Li B, et al.. Role of IgE-FcεR1 in pathological cardiac remodeling and dysfunction.Circulation. 2021; 143:1014–1030. doi: 10.1161/CIRCULATIONAHA.120.047852LinkGoogle Scholar2. Zhao H, Yang H, Geng C, Chen Y, Tang Y, Li Z, Pang J, Shu T, Nie Y, Liu Y, et al.. Elevated IgE promotes cardiac fibrosis by suppressing miR-486a-5p.Theranostics. 2021; 11:7600–7615. doi: 10.7150/thno.47845CrossrefMedlineGoogle Scholar3. Watkins SG, Dearin JL, Young LC, Wilhelm DI. Association of mastopoiesis with haemopoietic tissues in the neonatal rat.Experientia. 1976; 32:1339–1340. doi: 10.1007/BF01953127CrossrefMedlineGoogle Scholar4. Rakusan K, Sarkar K, Turek Z, Wicker P. Mast cells in the rat heart during normal growth and in cardiac hypertrophy.Circ Res. 1990; 66:511–516. doi: 10.1161/01.res.66.2.511LinkGoogle Scholar5. Sonoda T, Tsuyama K, Kitamura Y, Tanooka H. Different effects of dimethylbenz(alpha)anthracene and tetradecanoylphorbol acetate on differentiation of mast cells in the skin of mice.Am J Pathol. 1982; 106:312–317.MedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails September 28, 2021Vol 144, Issue 13Article InformationMetrics Download: 106 © 2021 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.121.055680PMID: 34570594 Originally publishedSeptember 27, 2021 PDF download SubjectsRemodelingThrombosis" @default.
- W3202040765 created "2021-10-11" @default.
- W3202040765 creator A5002217795 @default.
- W3202040765 creator A5006597480 @default.
- W3202040765 creator A5037677450 @default.
- W3202040765 creator A5055245284 @default.
- W3202040765 date "2021-09-28" @default.
- W3202040765 modified "2023-09-25" @default.
- W3202040765 title "Response by Zhao et al to Letter Regarding Article, “Role of IgE-FcεRI in Pathological Cardiac Remodeling and Dysfunction”" @default.
- W3202040765 cites W2017422781 @default.
- W3202040765 cites W2076329491 @default.
- W3202040765 cites W3112734310 @default.
- W3202040765 cites W3176899327 @default.
- W3202040765 doi "https://doi.org/10.1161/circulationaha.121.055680" @default.
- W3202040765 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34570594" @default.
- W3202040765 hasPublicationYear "2021" @default.
- W3202040765 type Work @default.
- W3202040765 sameAs 3202040765 @default.
- W3202040765 citedByCount "0" @default.
- W3202040765 crossrefType "journal-article" @default.
- W3202040765 hasAuthorship W3202040765A5002217795 @default.
- W3202040765 hasAuthorship W3202040765A5006597480 @default.
- W3202040765 hasAuthorship W3202040765A5037677450 @default.
- W3202040765 hasAuthorship W3202040765A5055245284 @default.
- W3202040765 hasBestOaLocation W32020407651 @default.
- W3202040765 hasConcept C161191863 @default.
- W3202040765 hasConcept C17744445 @default.
- W3202040765 hasConcept C191935318 @default.
- W3202040765 hasConcept C199539241 @default.
- W3202040765 hasConcept C2778304055 @default.
- W3202040765 hasConcept C2984488660 @default.
- W3202040765 hasConcept C2986762682 @default.
- W3202040765 hasConcept C3020610715 @default.
- W3202040765 hasConcept C41008148 @default.
- W3202040765 hasConcept C509550671 @default.
- W3202040765 hasConcept C71924100 @default.
- W3202040765 hasConceptScore W3202040765C161191863 @default.
- W3202040765 hasConceptScore W3202040765C17744445 @default.
- W3202040765 hasConceptScore W3202040765C191935318 @default.
- W3202040765 hasConceptScore W3202040765C199539241 @default.
- W3202040765 hasConceptScore W3202040765C2778304055 @default.
- W3202040765 hasConceptScore W3202040765C2984488660 @default.
- W3202040765 hasConceptScore W3202040765C2986762682 @default.
- W3202040765 hasConceptScore W3202040765C3020610715 @default.
- W3202040765 hasConceptScore W3202040765C41008148 @default.
- W3202040765 hasConceptScore W3202040765C509550671 @default.
- W3202040765 hasConceptScore W3202040765C71924100 @default.
- W3202040765 hasIssue "13" @default.
- W3202040765 hasLocation W32020407651 @default.
- W3202040765 hasLocation W32020407652 @default.
- W3202040765 hasOpenAccess W3202040765 @default.
- W3202040765 hasPrimaryLocation W32020407651 @default.
- W3202040765 hasRelatedWork W1488756026 @default.
- W3202040765 hasRelatedWork W1970449340 @default.
- W3202040765 hasRelatedWork W1985409980 @default.
- W3202040765 hasRelatedWork W2000928890 @default.
- W3202040765 hasRelatedWork W2084097346 @default.
- W3202040765 hasRelatedWork W2154113109 @default.
- W3202040765 hasRelatedWork W2278001431 @default.
- W3202040765 hasRelatedWork W2314490703 @default.
- W3202040765 hasRelatedWork W2389858093 @default.
- W3202040765 hasRelatedWork W3209085765 @default.
- W3202040765 hasVolume "144" @default.
- W3202040765 isParatext "false" @default.
- W3202040765 isRetracted "false" @default.
- W3202040765 magId "3202040765" @default.
- W3202040765 workType "article" @default.