Apoptosis-Like Cell Death Induction and Aberrant Fibroblast Properties in Human Incisional Hernia Fascia

Abstract

Incisional hernia often occurs following laparotomy and can be a source of serious problems. Although there is evidence that a biological cause may underlie its development, the mechanistic link between the local tissue microenvironment and tissue rupture is lacking. In this study, we used matched tissue-based and in vitro primary cell culture systems to examine the possible involvement of fascia fibroblasts in incisional hernia pathogenesis. Fascia biopsies were collected at surgery from incisional hernia patients and non-incisional hernia controls. Tissue samples were analyzed by histology and immunoblotting methods. Fascia primary fibroblast cultures were assessed at morphological, ultrastructural, and functional levels. We document tissue and fibroblast loss coupled to caspase-3 activation and induction of apoptosis-like cell-death mechanisms in incisional hernia fascia. Alterations in cytoskeleton organization and solubility were also observed. Incisional hernia fibroblasts showed a consistent phenotype throughout early passages in vitro, which was characterized by significantly enhanced cell proliferation and migration, reduced adhesion, and altered cytoskeleton properties, as compared to non-incisional hernia fibroblasts. Moreover, incisional hernia fibroblasts displayed morphological and ultrastructural alterations compatible with autophagic processes or lysosomal dysfunction, together with enhanced sensitivity to proapoptotic challenges. Overall, these data suggest an ongoing complex interplay of cell death induction, aberrant fibroblast function, and tissue loss in incisional hernia fascia, which may significantly contribute to altered matrix maintenance and tissue rupture in vivo.

Distinguish fatty acids impact survival, differentiation and cellular function of periodontal ligament fibroblasts

“…Our data suggest that palmitate treatment rather induce cellular senescence and cell death as cause for the diminished secretion of osteoclastogenesis-modulating factors. In particular, cells that are compromised in their survival due to external cues may not be able to properly perform their regulatory functions due to changes in their metabolism as well as their morphology and cellular contacts [70][71][72] . However, these results seems to be in contradiction with studies showing that palmitic acid enhances osteoclastic differentiation and activity 30 .…”

WITHDRAWN: Genome-wide association analysis of inguinal/scrotal hernia in pigs using specific length amplified fragment (SLAF) sequencing

“…According to previous studies, the failure of incomplete closure of processus vaginalis and internal inguinal ring was thought to play an important role in the development of inguinal hernias and scrotal hernias, respectively [48,49]. Both pathological appearances were caused by dysfunction of smooth muscle, which was , which is the key to programmed cell death [51]. In addition, abnormal collagen metabolism is strongly associated with hernia disease [52].…”

Bleichner’s hernia – lumbar hernia

“…Diaz et al used fibroblast cell culture techniques from fascial tissue samples from incisional hernia patients. They demonstrated aberrant fibroblast function and caspase –3 activation along with apoptotic signaling all leading to incisional hernia fascia tissue loss [5]. …”