Background: Microglandular hyperplasia (MGH) of the cervix in human beings is associated early with gland proliferation and terminates in mature squamous metaplasia. Using antibodies to basal cell markers, we analyzed biopsies with MGH to profile the distribution and evolution of reserve cells and their relationship to these epithelial components.
Design: Serial sections of 24 MGHs were subdivided into (1) early MGH with microacinar proliferation, abundant subnuclear vacuoles, and a paucity of supporting stroma and (2) late MGH with more prominent supporting stroma and/or squamous metaplasia. Serial sections were stained with antibodies to p63, bcl-2, and keratin-5.
Results: Three patterns of p63 staining were observed corresponding to the age of the MGH: (1) scattered staining of columnar cells, (2) focal subcolumnar staining in a reserve cell distribution, and (3) linear subcolumnar arrays of p63-positive reserve cells that in some MGHs expanded into a squamous metaplasia. Early acinar proliferations showed weak and focal columnar cell staining followed by focal subcolumnar p63-positive cells. In late lesions, p63 staining was compartmentalized to the extraglandular (or subcolumnar) areas. Stainings of p63, bcl-2, and keratin-5 were concordant. Staining for keratin 14, which localizes to squamous cells, was variable.
Conclusions: The immunohistochemical profile in MGH indicates that reserve cells are created in adulthood during specialized columnar proliferations. This columnar to reserve cell transition may produce a stable population of reserve cells or a transition to squamous metaplasia. Similar patterns are seen in cervical neoplasia, suggesting a link between benign and neoplastic cervical epithelial differentiation.
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http://dx.doi.org/10.1016/j.humpath.2004.10.017 | DOI Listing |
Ginekol Pol
January 2025
Department of Clinical Dietetics, Faculty of Health Sciences, Medical University of Warsaw, Poland, Poland.
Anti-Müllerian hormone (AMH), also known as Müller duct inhibitory factor and primarily known for its role in sexual differentiation. In female fetuses, AMH production by granulosa cells begins around the 36th week of gestation and continues in women until menopause. It is becoming more significant in the endocrine and gynecological diagnosis of adult women.
View Article and Find Full Text PDFElife
January 2025
Neurobiology and Genetics, Theodor-Boveri-Institute, Biocenter, Julius-Maximilians-University of Würzburg, Würzburg, Germany.
Insulin plays a key role in metabolic homeostasis. insulin-producing cells (IPCs) are functional analogues of mammalian pancreatic beta cells and release insulin directly into circulation. To investigate the in vivo dynamics of IPC activity, we quantified the effects of nutritional and internal state changes on IPCs using electrophysiological recordings.
View Article and Find Full Text PDFCell Death Discov
January 2025
Department of Ophthalmology and Visual Sciences, Case Western Reserve University, Cleveland, OH, USA.
Rhodopsin is the light-activated G protein-coupled receptor that initiates vision in photoreceptor cells of the retina. Numerous mutations in rhodopsin promote receptor misfolding and aggregation, causing autosomal dominant retinitis pigmentosa, a progressive retinal degenerative disease. The mechanism by which these mutations cause photoreceptor cell death, and the role aggregation plays in this process is still unclear.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Pediatric Surgical Research Laboratories, Massachusetts General Hospital, Boston, MA 02114.
Anti-Müllerian hormone (AMH) protects the ovarian reserve from chemotherapy, and this effect is most pronounced with Doxorubicin (DOX). However, DOX toxicity and AMH rescue mechanisms in the ovary have remained unclear. Herein, we characterize the consequences of these treatments in ovarian cell types using scRNAseq.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Otolaryngology, Case Western Reserve University, Cleveland, OH, 44106, USA.
Usher syndrome type 1C (USH1C) is a genetic disorder caused by mutations in the USH1C gene, which encodes harmonin, a key component of the mechanoelectrical transduction complex in auditory and vestibular hair cells. USH1C leads to deafness and vestibular dysfunction in humans. An Ush1c knockout (KO) mouse model displaying these characteristic deficits is generated in our laboratory.
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