scholarly journals Consumption of a Blueberry-Enriched Diet by Women for 6 Weeks Alters Determinants of Human Muscle Progenitor Cell Function

2020 ◽  
Vol 150 (9) ◽  
pp. 2412-2418 ◽  
Author(s):  
Jamie E Blum ◽  
Brandon J Gheller ◽  
Sinwoo Hwang ◽  
Erica Bender ◽  
Mary Gheller ◽  
...  

ABSTRACT Background Human muscle progenitor cell (hMPC) function facilitates skeletal muscle regeneration and is influenced by circulating factors. Yet it is unknown whether dietary interventions impact hMPC function. Blueberry consumption was examined due to the pro-proliferative and antioxidant effects of blueberries and blueberry-derived compounds. Objectives This study measured indicators of hMPC function in young and old cultures treated with serum collected from a blueberry-enriched diet (BED) intervention. Methods Younger (21–40 y, n = 12) and older (60–79 y, n = 10) women consumed a 6-wk BED (38 g of freeze-dried blueberries daily). Fasting serum was collected at 0, 4, and 6 wk, and a fed serum sample at 1.5 h (acute) after starting the BED intervention. Young and old hMPCs, derived from 3–5 distinct donors (biological replicates), were individually cultured in media containing pooled, age-group–matched serum from each time point. Determinants of hMPC function (e.g., hMPC number, oxidative stress resistance, and upregulation of metabolic pathways) were measured and compared within age groups. Results Culturing young hMPCs in acute (compared with 0 wk) BED serum did not alter hMPC number or oxidative stress–induced cell death, but increased cellular oxygen consumption (29%, P = 0.026). Culturing young hMPCs in 6-wk (compared with 0-wk) BED serum increased hMPC number (40%, P = 0.0024), conferred minor resistance to oxidative stress–induced cell death (12.6 percentage point decrease, P = 0.10), and modestly increased oxygen consumption (36%, P = 0.09). No beneficial effect of the acute or long-term BED serum was observed in old hMPCs. Conclusions In younger women, dietary interventions could be a feasible strategy to improve hMPC function and thus muscle regeneration, through altering the serum environment. This study was registered at clinicaltrials.gov (NCT04262258).

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0159411 ◽  
Author(s):  
Keith G. Avin ◽  
Neal X. Chen ◽  
Jason M. Organ ◽  
Chad Zarse ◽  
Kalisha O’Neill ◽  
...  

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Addolorata Pisconti ◽  
Glen B. Banks ◽  
Farshad Babaeijandaghi ◽  
Nicole Dalla Betta ◽  
Fabio M. V. Rossi ◽  
...  

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Xiaoguang Liu ◽  
Weihua Xiao ◽  
Lifang Zhen ◽  
Yongzhan Zhou ◽  
Jian Shou

Objective Skeletal muscle contusion is one of the most common muscle injury in sports medicine and traumatology. Bone marrow mesenchymal stem cells (BMSCs) transplantation is a promising strategy for muscle regeneration. However, the roles of BMSCs, especially the mechanisms involved, in the regeneration of contused skeletal muscle are still not fully recognized. The aim of the study is to evaluate the potential of BMSCs transplantation for muscle regeneration and mechanisms involved after contusion. Methods Ninety-nine C57BL/6J mice were divided into three groups: control group (n=11), muscle contusion and BMSCs treated group (n=44), muscle contusion and sham treated group (n=44). BMSCs were immediately transplanted into gastrocnemius muscles (GMs) following direct contusion. At different time points (3, 6, 12 and 24 days) post-injury, the animals were killed and then GMs were harvested. Morphological and gene expression analyses were used to elevate the effect of BMSCs transplantation and mechanisms involved. Results The results indicate that BMSCs transplantation impairs muscle regeneration, as well as more fibrotic scar formation after skeletal muscle contusion. Furthermore, macrophages, inflammatory cytokines, chemokines, matrix metalloproteinases and oxidative stress related enzymes were significantly increased after BMSCs transplantation. These results suggest that BMSCs transplantation impairs skeletal muscle regeneration and that macrophages, inflammatory cytokines, chemokines, matrix metalloproteinases and oxidative stress related enzymes may be involved in the process. Conclusions BMSCs transplantation aggravates inflammation, oxidative stress and fibrosis, and impairs skeletal muscle regeneration, which shed new light on the role of BMSCs in regenerative medicine and cautions the application of BMSCs for muscle injury.


2019 ◽  
Vol 10 ◽  
Author(s):  
Xiaoguang Liu ◽  
Lifang Zheng ◽  
Yongzhan Zhou ◽  
Yingjie Chen ◽  
Peijie Chen ◽  
...  

2007 ◽  
Vol 282 (43) ◽  
pp. 31453-31459 ◽  
Author(s):  
Germana Zaccagnini ◽  
Fabio Martelli ◽  
Alessandra Magenta ◽  
Chiara Cencioni ◽  
Pasquale Fasanaro ◽  
...  

PLoS ONE ◽  
2011 ◽  
Vol 6 (3) ◽  
pp. e17454 ◽  
Author(s):  
Jinhong Meng ◽  
Carl F. Adkin ◽  
Shi-wen Xu ◽  
Francesco Muntoni ◽  
Jennifer E. Morgan

2021 ◽  
Vol 22 (11) ◽  
pp. 5491
Author(s):  
Yuya Takahashi ◽  
Tatsunori Shimizu ◽  
Shunsuke Kato ◽  
Mitsuhiko Nara ◽  
Yumi Suganuma ◽  
...  

Superoxide dismutase (SOD) is a major antioxidant enzyme for superoxide removal, and cytoplasmic SOD (SOD1) is expressed as a predominant isoform in all cells. We previously reported that renal SOD1 deficiency accelerates the progression of diabetic nephropathy (DN) via increasing renal oxidative stress. To evaluate whether the degree of SOD1 expression determines regeneration capacity and sarcopenic phenotypes of skeletal muscles under incipient and advanced DN conditions, we investigated the alterations of SOD1 expression, oxidative stress marker, inflammation, fibrosis, and regeneration capacity in cardiotoxin (CTX)-injured tibialis anterior (TA) muscles of two Akita diabetic mouse models with different susceptibility to DN, DN-resistant C57BL/6-Ins2Akita and DN-prone KK/Ta-Ins2Akita mice. Here, we report that KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, exhibit delayed muscle regeneration after CTX injection, as demonstrated by the finding indicating significantly smaller average cross-sectional areas of regenerating TA muscle myofibers relative to KK/Ta-wild-type mice. Furthermore, we observed markedly reduced SOD1 expression in CTX-injected TA muscles of KK/Ta-Ins2Akita mice, but not C57BL/6-Ins2Akita mice, along with increased inflammatory cell infiltration, prominent fibrosis and superoxide overproduction. Our study provides the first evidence that SOD1 reduction and the following superoxide overproduction delay skeletal muscle regeneration through induction of overt inflammation and fibrosis in a mouse model of progressive DN.


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