Research output: Contribution to journal › Article › peer-review
Restraint Stress-Induced Expression of Fos and Several Related Genes in the Hypothalamus of Hypertensive ISIAH Rats. / Makovka, Y. V.; Fedoseeva, L. A.; Oshchepkov, D. Yu et al.
In: Molecular Biology, Vol. 58, No. 1, 02.2024, p. 62-70.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Restraint Stress-Induced Expression of Fos and Several Related Genes in the Hypothalamus of Hypertensive ISIAH Rats
AU - Makovka, Y. V.
AU - Fedoseeva, L. A.
AU - Oshchepkov, D. Yu
AU - Markel, A. L.
AU - Redina, O. E.
N1 - This work was supported by the Russian Science Foundation (project no. 22-14-00082).
PY - 2024/2
Y1 - 2024/2
N2 - Stress can play a significant role in arterial hypertension and many other complications of cardiovascular diseases. Considerable attention is paid to the study of the molecular mechanisms involved in the body response to stressful influences, but there are still many blank spots in understanding the details. ISIAH rats model the stress-sensitive form of arterial hypertension. ISIAH rats are characterized by genetically determined enhanced activities of the hypothalamic–pituitary–adrenocortical and sympathetic–adrenomedullary systems, suggesting a functional state of increased stress reactivity. For the first time, the temporal expression patterns of Fos and several related genes were studied in the hypothalamus of adult male hypertensive ISIAH rats after a single exposure to restraint stress for 30, 60, or 120 min. Fos transcription was activated and peaked 1 h after the start of restraint stress. The time course of Fos activation coincided with that of blood pressure increase after stress. Activation of hypothalamic neurons also alters the transcription levels of several transcription factor genes (Jun, Nr4a3, Jdp2, and Ppargc1a), which are associated with the development of cardiovascular diseases. Because Fos induction is a marker of brain neuron activation, activation of hypothalamic neurons and an increase in blood pressure were concluded to accompany increased stress reactivity of the hypothalamic–pituitary–adrenocortical and sympathoadrenal systems in hypertensive ISIAH rats during short-term restraint.
AB - Stress can play a significant role in arterial hypertension and many other complications of cardiovascular diseases. Considerable attention is paid to the study of the molecular mechanisms involved in the body response to stressful influences, but there are still many blank spots in understanding the details. ISIAH rats model the stress-sensitive form of arterial hypertension. ISIAH rats are characterized by genetically determined enhanced activities of the hypothalamic–pituitary–adrenocortical and sympathetic–adrenomedullary systems, suggesting a functional state of increased stress reactivity. For the first time, the temporal expression patterns of Fos and several related genes were studied in the hypothalamus of adult male hypertensive ISIAH rats after a single exposure to restraint stress for 30, 60, or 120 min. Fos transcription was activated and peaked 1 h after the start of restraint stress. The time course of Fos activation coincided with that of blood pressure increase after stress. Activation of hypothalamic neurons also alters the transcription levels of several transcription factor genes (Jun, Nr4a3, Jdp2, and Ppargc1a), which are associated with the development of cardiovascular diseases. Because Fos induction is a marker of brain neuron activation, activation of hypothalamic neurons and an increase in blood pressure were concluded to accompany increased stress reactivity of the hypothalamic–pituitary–adrenocortical and sympathoadrenal systems in hypertensive ISIAH rats during short-term restraint.
KW - ISIAH rat strain
KW - hypothalamus
KW - immediate early genes
KW - single restraint stress exposure
UR - https://www.scopus.com/record/display.uri?eid=2-s2.0-85187104760&origin=inward&txGid=92a3c50776a0c3b2f5058bb43d23b532
UR - https://www.webofscience.com/wos/woscc/full-record/WOS:001177617100004
UR - https://www.mendeley.com/catalogue/b3738e40-f0a1-35be-8af7-d6a14318d819/
U2 - 10.1134/S0026893324010072
DO - 10.1134/S0026893324010072
M3 - Article
VL - 58
SP - 62
EP - 70
JO - Molecular Biology
JF - Molecular Biology
SN - 0026-8933
IS - 1
ER -
ID: 61166968