Fate Tracing of Isl1+Cells in Adult Mouse Hearts under Physiological and Exercise Conditions

2019 ◽  
Vol 40 (14) ◽  
pp. 921-930
Author(s):  
Yunhe Zhou ◽  
Hua Yang ◽  
Jiahao Shi ◽  
Mengjie Zhang ◽  
Sai Yang ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Atrioventricular Node ◽  
Myocardial Damage ◽  
Heart Cell ◽  
Cardiomyocyte Proliferation ◽  
Adult Mice ◽  
Cardiac Ganglia ◽  
Early Mouse ◽  
Response To Exercise

AbstractMyocardial damage due to dysfunctional myocardium has been increasing, and the prognosis of pharmacological and device-based therapies remain poor. Isl1-expressing cells were thought to be progenitor cells for cardiomyocyte proliferation after specific stimuli. However, the true origin of the proliferating myocardiac cells and the role of Isl1 in adult mammals remain unresolved. In this study, Isl1-CreERT2 knock-in mouse model was constructed using CRISPR/Cas9 technology. Using tamoxifen-inducible Isl1-CreERT/Rosa26R-LacZ system, Isl1+cells and their progeny were permanently marked by lacZ-expression. X-gal staining, immunostaining, and quantitative PCR were then used to reveal the fate of Isl1+cells under physiological and exercise conditions in mouse hearts from embryonic stage to adulthood. Isl1+cells were found to localize to the sinoatrial node, atrioventricular node, cardiac ganglia, aortic arch, and pulmonary roots in adult mice heart. However, they did not act as cardiac progenitor cells under physiological and exercise conditions. Although Isl1+cells showed progenitor cell properties in early mouse embryos (E7.5), this ability was lost by E9.5. Furthermore, although the proliferation and regeneration of heart cell was observed in response to exercise, the cells associated were not Isl1 positive.

scholarly journals Deletion of mouseSetd4promotes the recovery of hematopoietic failure

2019 ◽  
Author(s):  
Xing Feng ◽  
Huimei Lu ◽  
Jingyin Yue ◽  
Megha Shettigar ◽  
Jingmei Liu ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Progenitor Cells ◽  
Whole Body ◽  
List Type ◽  
Bone Marrow Niche ◽  
Hematopoietic Stem ◽  
Adult Mice ◽  
Bm Niche ◽  
Deficient Mice

AbstractAcquired hematopoietic failure is commonly caused by therapeutic and accidental exposure to toxic agents to the bone marrow (BM). Efficient recovery from the BM failure is not only dictated by the intrinsic sensitivity and proliferation capacity of the hematopoietic stem and progenitor cells, but also nourished by the BM environment niche. Identification of genetic factors that improve the recovery from hematopoietic failure is essential. Vertebrate SETD4 is a poorly characterized, putative non-histone methyl-transferase whose physiological substrates have not yet been fully identified. By inducingSetd4deletion in adult mice, we found that loss ofSetd4improved the survival of whole body irradiation induced BM failure. This was associated with improved recoveries of long-term and short-term hematopoietic stem cells (HSC), and early progenitor cells. BM transplantation analyses surprisingly showed that the improved recovery was not due to a radiation resistance of theSetd4deficient HSC, but thatSetd4deficient HSC were actually more sensitive to radiation. However, theSetd4deficient mice were better recipients for allogeneic HSC transplantation. Furthermore, there was an enhanced splenic erythropoiesis inSetd4deficient mice. These findings not only revealed a previously unrecognized role of theSetd4as a unique modulator of hematopoiesis, but also underscored the critical role of the BM niche in the recovery of hematopoietic failure. These studies also implicatedSetd4as a potential target for therapeutic inhibition to improve the conditioning of the BM niche prior to allogeneic transplantation.Key pointsDeletion ofSetd4in adult mice improved the survival from hematopoietic failure.Setd4deficiency sensitized HSCs to radiation, but improved bone marrow environment niche.The study suggests that SETD4 as a potential inhibitory target to improve bone marrow niche function for recovery of bone marrow failure.

Differentiation of chromaffin progenitor cells: Possible role of DHEA and DHEAS

2007 ◽  
Vol 115 (S 1) ◽  
Author(s):  
KF Chung ◽  
F Sicard ◽  
S Sperber ◽  
D Corbeil ◽  
AW Krug ◽  
...  
Keyword(s):  
Progenitor Cells

1962-P: Role of Transcription Factor TCF21 in Adipocyte Progenitor Cells of Visceral Fat

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1962-P
Author(s):  
TAKUYA MINAMIZUKA ◽  
YOSHIRO MAEZAWA ◽  
HARUHIDE UDAGAWA ◽  
YUSUKE BABA ◽  
MASAYA KOSHIZAKA ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Progenitor Cells ◽  
Visceral Fat

Catecholamine-fuel interrelationships during exercise in fasting men

1980 ◽  
Vol 48 (1) ◽  
pp. 109-113 ◽  
Author(s):  
J. M. Pequignot ◽  
L. Peyrin ◽  
G. Peres
Keyword(s):  
Maximal Oxygen Consumption ◽  
Plasma Catecholamines ◽  
Plasma Free Fatty Acid ◽  
Work Load ◽  
Bicycle Ergometer ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Adrenergic Response ◽  
Response To Exercise

Adrenergic response to exercise and the relationships between plasma catecholamines and blood energetic substrates were studied in sedentary men after 15 h of fasting. Subjects pedaled a bicycle ergometer until exhaustion at a work load approximating 80% maximal oxygen consumption. Working ability was diminished by the fast (P less than 0.025). Resting plasma norepinephrine level was increased by fasting. During exercise plasma epinephrine (E) and norepinephrine (NE) concentrations were more elevated in fasting subjects than in fed subjects. Plasma catecholamine (CA) levels in fasting men correlated with blood glucose, blood lactate, and plasma glycerol concentrations. There was no significative correlation between CA and plasma free fatty acid (FFA) levels. The increased adrenergic activity in fasting subjects correlated with reduced endurance time. This study emphasizes the role of CA release, probably combined with other hormonal factors, in the mobilization of energy substrates during submaximal exercise.

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