Studies from Tohoku University Reveal New Findings on Chronic Obstructive Pulmonary Disease (Decrease in an anti-ageing factor, growth differentiation factor 11, in chronic obstructive pulmonary disease)
By a News Reporter-Staff News Editor at Genomics & Genetics Weekly -- Research findings on Lung Diseases and Conditions - Chronic Obstructive Pulmonary Disease are discussed in a new report. According to news reporting out of Miyagi, Japan, by NewsRx editors, research stated, "Cellular senescence is observed in the lungs of patients with COPD and may contribute to the disease pathogenesis. Growth differentiation factor 11 (GDF11) belongs to the transforming growth factor beta superfamily and was recently reported to be a circulating protein that may have rejuvenating effects in mice."
Our news journalists obtained a quote from the research from Tohoku University, "We aimed to investigate the amounts of GDF11 in the plasma and the lungs of patients with COPD and elucidate the possible roles of GDF11 in cellular senescence. The plasma levels of GDF11 were investigated in two separate cohorts by western blotting. The localisation and expression of GDF11 in the lungs were investigated by immunohistochemistry and quantitative reverse transcription PCR, respectively. The effects of GDF11 on both cigarette smoke extract (CSE)-induced cellular senescence in vitro and on elastase-induced cellular senescence in vivo were investigated. The levels of plasma GDF11 in the COPD group were decreased compared with the control groups in the two independent cohorts. The levels of plasma GDF11 were significantly positively correlated with pulmonary function data. The mRNA expression of GDF11 in mesenchymal cells from the COPD group was decreased. Chronic exposure to CSE decreased the production of GDF11. Treatment with GDF11 significantly inhibited CSE-induced cellular senescence and upregulation of inflammatory mediators, partly through Smad2/3 signalling in vitro. Daily GDF11 treatment attenuated cellular senescence and airspace enlargement in an elastase-induced mouse model of emphysema."
According to the news editors, the research concluded: "The decrease in GDF11 may be involved in the cellular senescence observed in COPD."
For more information on this research see: Decrease in an anti-ageing factor, growth differentiation factor 11, in chronic obstructive pulmonary disease. Thorax, 2017;72(10):893-904. Thorax can be contacted at: Bmj Publishing Group, British Med Assoc House, Tavistock Square, London WC1H 9JR, England. (BMJ Publishing Group - group.bmj.com/; Thorax - thorax.bmj.com/)
Our news journalists report that additional information may be obtained by contacting H. Sugiura, Tohoku University, Dept. of Resp Med, Grad Sch Med, Sendai, Miyagi, Japan. Additional authors for this research include K. Onodera, M. Yamada, A. Koarai, N. Fujino, S. Yanagisawa, R. Tanaka, T. Numakura, S. Togo, K. Sato, Y. Kyogoku, Y. Hashimoto, T. Okazaki, T. Tamada, S. Kobayashi, M. Yanai, M. Miura, Y. Hoshikawa, Y. Okada, S. Suzuki and Ic (see also Lung Diseases and Conditions - Chronic Obstructive Pulmonary Disease).
The direct object identifier (DOI) for that additional information is: https://doi.org/10.1136/thoraxjnl-2016-209352. This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.
Keywords for this news article include: Miyagi, Japan, Asia, Intercellular Signaling Peptides and Proteins, Chronic Obstructive Pulmonary Disease, Growth Differentiation Factors, TGF-beta Superfamily Proteins, Lung Diseases and Conditions, Enzymes and Coenzymes, Elastase, Genetics, Tohoku University.
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