Chronic stress exposure and daily stress appraisals relate to biological aging marker p16INK4a

Abstract

Previous research has linked exposure to adverse social conditions with DNA damage and accelerated telomere shortening, raising the possibility that chronic stress may impact biological aging pathways, ultimately increasing risk for age-related diseases. Less clear, however, is whether these stress-related effects extend to additional hallmarks of biological aging, including cellular senescence, a stable state of cell cycle arrest. The present study aimed to investigate associations between psychosocial stress and two markers of cellular aging-leukocyte telomere length (LTL) and cellular senescence signal p16 INK4a. Seventy-three adults (M age = 43.0, SD = 7.2; 55% female) with children between 8-13 years of age completed interview-based and questionnaire measures of their exposures to and experiences of stress, as well as daily reports of stress appraisals over an 8-week diary period. Blood samples were used to assess markers of cellular aging: LTL and gene expression of senescent cell signal p16 INK4a (CDKN2A). Random effects models covarying for age, sex, ethnicity/race, and BMI revealed that participants with greater chronic stress exposure over the previous 6 months (b = 0.011, p = .04), perceived stress (b = 0.020, p < .001), and accumulated daily stress appraisals over the 8-week period (b = 0.013, p = .

Relationship closeness buffers the effects of perceived stress on transcriptomic indicators of cellular stress and biological aging marker p16INK4a

“…In addition, whereas previous studies of the stressbuffering effects of parent-child relationships and biological aging have relied on retrospective reports of stress and parental warmth in childhood, this study involves concurrent assessment of psychosocial stress using multiple methods (interview-based, selfreport, and intensive repeated measures over 56 days), relationship closeness, and biological aging in a sample of midlife parents. Based on evidence of the stress-buffering effects of high-quality and supportive relationships, we extend our previous findings [12] by hypothesizing that parents who experience less closeness with their spouse will show stronger associations between psychosocial stress and expression of the p16 INK4a -encoding gene (CDKN2A) than those with greater closeness. A secondary aim of the study is to explore upstream transcription control pathways activated under cell stress (Nrf2, HSF-1 and HSF-2); however, the extant literature is not sufficiently developed to inform directional hypotheses.…”

“…Unresolved or prolonged cell stress can lead to excess DNA damage and initiate a permanent state of cell growth arrest termed cellular senescence [10,11]. Whether psychosocial stress exposures lead to cellular senescence is unclear, although our initial cross-sectional findings have linked chronic stress exposure, perceived stress and accumulated daily stress appraisals to increased expression of cell cycle inhibitor p16 INK4a , a marker of cellular senescence in peripheral blood cells [12].…”

“…Several variables that might affect the number of leukoctyes in circulation and estimates of CDKN2A expression were evaluated as potential covariates in the main analyses based on previous research [12,29,34] [13]. Cell subsets were obtained by complete blood count with differential assessed by the UCLA Clinical Laboratory and Pathology Services using standard clinical laboratory methods.…”

Phenytoin sodium‐ameliorated gingival fibroblast aging is associated with autophagy

“…P16 INK4A and P21 cip1 are key effectors of cell aging, can prevent G0/G1 period cell from entering proliferation cycle, and induce aging progression 34,35 . H 2 O 2 ‐induced HGF‐1 cells increased the expression levels of P16 INK4A and P21 cip1 genes and proteins, aggrandizing the G1 proportion in the cell cycle.…”

Clinical and Immunological Features of Secondary Immunodeficiency in the Forced Inhabitants of Donetsk Region Displaced from the Military Operations Area

“…У части пациентов стрессорная иммунная недостаточность протекает в латентном субклиническом виде, имеет обратимый характер и компенсируется после реабилитационных мероприятий. В то же время, значительная часть пациентов отмечает стойкие декомпенсированные нарушения иммунной системы с развитием патологических явлений, которые требуют не только проведения лечения у врачей различного профиля, но и обязательно иммунокоррекции, что вынуждает их обращаться к специалистуклиническому иммунологу [1,2].…”