Long noncoding RNA H 19 mediates melatonin inhibition of premature senescence of c‐kit+ cardiac progenitor cells by promoting mi R‐675

Cai, Benzhi; Ma, Wenya; Bi, Chongwei; Yang, Fan; Zhang, Lai; Han, Zhenbo; Huang, Qi; Ding, Fengzhi; Li, Yuan; Yan, Gege; Pan, Zhenwei; Yang, Baofeng; Lu, Yanjie

doi:10.1111/jpi.12331

Cited by 98Telomeres, Telomerase, and SenescenceCircadian rhythm and melatoninMesenchymal stem cell research

Long noncoding RNA H 19 mediates melatonin inhibition of premature senescence of c‐kit+ cardiac progenitor cells by promoting mi R‐675

Cai, Benzhi, Ma, Wenya, Bi, Chongwei, Yang, Fan, Zhang, Lai, Han, Zhenbo, Huang, Qi, Ding, Fengzhi +5 more·2016·Journal of Pineal Research

DOI 10.1111/jpi.12331

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Abstract

Melatonin, a hormone secreted by the pineal gland, possesses multiple biological activities such as antitumor, antioxidant, and anti‐ischemia. C‐kit+ cardiac progenitor cells (CPC s) have emerged as a promising tool for the treatment of heart diseases. However, the senescence of CPC s due to pathological stimuli leads to the decline of CPC s' functions and regenerative potential. This study was conducted to demonstrate whether melatonin antagonizes the senescence of CPC s in response to oxidative stress. Here, we found that the melatonin treatment markedly inhibited the senescent characteristics of CPC s after exposed to sublethal concentration of H 2 O 2, including the increase in senescence‐associated β‐galactosidase (SA‐β‐gal)‐positive CPC s, senescence‐associated heterochromatin loci (SAHF), secretory IL‐6 level, and the upregulation of p53 and p21 proteins. Senescence‐associated proliferation reduction was also attenuated by melatonin in CPC s. Luzindole, the melatonin membrane receptor blocker, may block the melatonin‐mediated suppression of premature senescence in CPC s. Interestingly, we found that long noncoding RNA H19 and its derived miR‐675 were downregulated by H 2 O 2 in CPC s, but melatonin treatment could counter this alteration. Furthermore, knockdown of H19 or miR‐675 blocked antisenescence actions of melatonin on H 2 O 2‐treated CPC s. It was further verified that H19‐derived miR‐675 targeted at the 3′UTR of USP 10, which resulted in the downregulation of p53 and p21 proteins. In summary, melatonin antagonized premature senescence of CPC s via H19/miR‐675/USP 10 pathway, which provides new insights into pharmacological actions and potential applications of melatonin on the senescence of CPC s.

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Melatonin decreases p53, p21, and p16 proteins and enhances SIRT1 activity in H2O2-induced senescence.
“Melatonin-induced decrease in p53, p21 and p16 proteins, together with enhanced SIRT1 activity, have also been reported in the context of H2O2-induced senescence [458,459].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [458]

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Authors: Cai, B., Ma, W., Bi, C., Yang, F., Zhang, L., Han, Z., Huang, Q., Ding, F., Li, Y., Yan, G., Pan, Z., Yang, B., & Lu, Y.
Affiliations: Harbin Medical University (CN)
Corresponding author: Cai, Benzhi
Yang, Baofeng
ORCID: Cai, Benzhi
Ma, Wenya
Yang, Fan
Zhang, Lai
Han, Zhenbo
Huang, Qi
Ding, Fengzhi
Li, Yuan
Yan, Gege
Pan, Zhenwei
Yang, Baofeng
Venue: Journal of Pineal Research
Publisher: Wiley
Published: 2016-04-29
Volume: 61
Issue: 1
Pages: 82-95
ISSN: 0742-3098 (ISSN-L)
1600-079X
DOI: 10.1111/jpi.12331
OpenAlex: W2335004067
Cited by: 98
References: 55
Citations by year: 2025: 1 · 2024: 6 · 2023: 4 · 2022: 10 · 2021: 18 · 2020: 10 · 2019: 16 · 2018: 24 · 2017: 8 · 2016: 1
FWCI: 13.15
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Journal of Pineal Research (publishedVersion)
PubMed (publishedVersion)
Funders: National Natural Science Fund of China (81170096/81573434)
Program for New Century Excellent Talents in Heilongjiang Provincial Universities (1252-NCET-013)
Young Creative Talents Training Program of Heilongjiang Provincial Universities
Topics: Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
Keywords: melatonin, premature senescence, cardiac progenitor cells, c-kit+ cells, long non-coding RNA H19, miR-675, USP10, oxidative stress, hydrogen peroxide, p53, p21, senescence-associated β-galactosidase, senescence-associated heterochromatin foci, interleukin-6, luzindole, melatonin receptors, cardiac regeneration
MeSH terms: Animals, Hydrogen Peroxide, Melatonin, Stem Cells, Cellular Senescence, Proto-Oncogene Proteins c-kit, 3' Untranslated Regions, Myocytes, Cardiac, MicroRNAs, Ubiquitin Thiolesterase, Mice, Gene Knockdown Techniques, RNA, Long Noncoding

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Long noncoding RNA H 19 mediates melatonin inhibition of premature senescence of c‐kit+ cardiac progenitor cells by promoting mi R‐675

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