Precocious glucocorticoid exposure reduces skeletal muscle satellite cells in the fetal rat
© 2017 Society for Endocrinology..
Perinatal skeletal muscle growth rates are a function of protein and myonuclear accretion. Precocious exposure of the fetus to glucocorticoids (GLC) in utero impairs muscle growth. Reduced muscle protein synthesis rates contribute to this response, but the consequences for myonuclear hyperplasia are unknown. To test the hypothesis that blunting of Pax7+ muscle progenitor cell proliferative activity by GLC in vivo also contributes to reduced fetal muscle growth, pregnant rats were administered dexamethasone (DEX: 1 mg/L drinking water) from embryonic day (ED) 13 to ED21. Their responses were compared to pair-fed (PF) and ad libitum-fed controls (CON). Bromodeoxyuridine (BrdU) was administered before delivery to measure myonuclear accretion. Fetal hind limb and diaphragm muscles were collected at term and analyzed for myofiber cross-sectional area (CSA), total and BrdU+ myonuclei, Pax7+ nuclei, MyoD and myogenin protein and mRNA abundance and myosin heavy chain (MyHC) isoform composition. Mean fiber CSA, myonuclei/myofiber and Pax7+ nuclei/myofiber ratios were reduced in DEX compared to those in CON and PF muscles; CSA/myonucleus, BrdU+/total myonuclei and BrdU+ myonuclei/Pax7+ nuclei were similar among groups. Myogenin abundance was reduced and MyHC-slow was increased in DEX fetuses. The data are consistent with GLC inhibition of muscle progenitor cell proliferation limiting satellite cell and myonuclear accretion. The response of PF-fed compared to CON muscles indicated that decreased food consumption by DEX dams contributed to the smaller myofiber CSA but did not affect Pax7+ nuclear accretion. Thus, the effect on satellite cell reserve and myonuclear number also contributes to the blunting of fetal muscle growth by GLC.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2017 |
|---|---|
| Erschienen: |
2017 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:232 |
|---|---|
| Enthalten in: |
The Journal of endocrinology - 232(2017), 3 vom: 15. März, Seite 561-572 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Gokulakrishnan, Ganga [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 20.06.2017 Date Revised 13.11.2018 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1530/JOE-16-0372 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM26808601X |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM26808601X | ||
| 003 | DE-627 | ||
| 005 | 20231224222008.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231224s2017 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1530/JOE-16-0372 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0893.xml |
| 035 | |a (DE-627)NLM26808601X | ||
| 035 | |a (NLM)28096434 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Gokulakrishnan, Ganga |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Precocious glucocorticoid exposure reduces skeletal muscle satellite cells in the fetal rat |
| 264 | 1 | |c 2017 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 20.06.2017 | ||
| 500 | |a Date Revised 13.11.2018 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2017 Society for Endocrinology. | ||
| 520 | |a Perinatal skeletal muscle growth rates are a function of protein and myonuclear accretion. Precocious exposure of the fetus to glucocorticoids (GLC) in utero impairs muscle growth. Reduced muscle protein synthesis rates contribute to this response, but the consequences for myonuclear hyperplasia are unknown. To test the hypothesis that blunting of Pax7+ muscle progenitor cell proliferative activity by GLC in vivo also contributes to reduced fetal muscle growth, pregnant rats were administered dexamethasone (DEX: 1 mg/L drinking water) from embryonic day (ED) 13 to ED21. Their responses were compared to pair-fed (PF) and ad libitum-fed controls (CON). Bromodeoxyuridine (BrdU) was administered before delivery to measure myonuclear accretion. Fetal hind limb and diaphragm muscles were collected at term and analyzed for myofiber cross-sectional area (CSA), total and BrdU+ myonuclei, Pax7+ nuclei, MyoD and myogenin protein and mRNA abundance and myosin heavy chain (MyHC) isoform composition. Mean fiber CSA, myonuclei/myofiber and Pax7+ nuclei/myofiber ratios were reduced in DEX compared to those in CON and PF muscles; CSA/myonucleus, BrdU+/total myonuclei and BrdU+ myonuclei/Pax7+ nuclei were similar among groups. Myogenin abundance was reduced and MyHC-slow was increased in DEX fetuses. The data are consistent with GLC inhibition of muscle progenitor cell proliferation limiting satellite cell and myonuclear accretion. The response of PF-fed compared to CON muscles indicated that decreased food consumption by DEX dams contributed to the smaller myofiber CSA but did not affect Pax7+ nuclear accretion. Thus, the effect on satellite cell reserve and myonuclear number also contributes to the blunting of fetal muscle growth by GLC | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Research Support, N.I.H., Extramural | |
| 650 | 4 | |a Research Support, U.S. Gov't, Non-P.H.S. | |
| 650 | 4 | |a food restriction | |
| 650 | 4 | |a hypertrophy | |
| 650 | 4 | |a muscle regulatory factors | |
| 650 | 4 | |a myosin | |
| 650 | 4 | |a skeletal muscle | |
| 650 | 7 | |a Glucocorticoids |2 NLM | |
| 650 | 7 | |a Myogenin |2 NLM | |
| 650 | 7 | |a PAX7 protein, rat |2 NLM | |
| 650 | 7 | |a Paired Box Transcription Factors |2 NLM | |
| 650 | 7 | |a Dexamethasone |2 NLM | |
| 650 | 7 | |a 7S5I7G3JQL |2 NLM | |
| 650 | 7 | |a Myosin Heavy Chains |2 NLM | |
| 650 | 7 | |a EC 3.6.4.1 |2 NLM | |
| 700 | 1 | |a Chang, Xiaoyan |e verfasserin |4 aut | |
| 700 | 1 | |a Fleischmann, Ryan |e verfasserin |4 aut | |
| 700 | 1 | |a Fiorotto, Marta L |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t The Journal of endocrinology |d 1946 |g 232(2017), 3 vom: 15. März, Seite 561-572 |w (DE-627)NLM000005894 |x 1479-6805 |7 nnns |
| 773 | 1 | 8 | |g volume:232 |g year:2017 |g number:3 |g day:15 |g month:03 |g pages:561-572 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1530/JOE-16-0372 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 232 |j 2017 |e 3 |b 15 |c 03 |h 561-572 | ||