Retinoic acid (RA) plays a critical role in normal development and tissue maintenance and is also a regulatory factor of anterior pituitary cells. We previously demonstrated that a retinoic acid-synthesizing enzyme, retinaldehyde dehydrogenase 1 (RALDH1), is expressed in prolactin cells of adult rats and that estrogen suppressed RALDH1 expression. It is suggested that RA plays a role as a paracrine and/or autocrine signaling molecule in the anterior pituitary gland. However, the presence of RALDH1 in pituitary tumors has not been demonstrated. In this study, we examined the expression of RALDH1 in diethylstilbestrol-induced prolactinoma of LEXF RI rats. Quantitative analysis of mRNA levels by real-time PCR demonstrated drastic reduction of RALDH1 expression in the prolactinoma. We have also detected both mRNA expression and production by in situ hybridization and immunohistochemistry. Both mRNA-expressing cells and immunopositive cells remarkably decreased after 4 weeks of treatment with diethylstilbestrol. Fluorescence double immunohistochemistry of RALDH1 and prolactin revealed that prolactin-immunopositive cells do not colocalize with RALDH1 in the prolactinoma. These results suggest that the reduction of local RA generation relates to cell proliferation and tumorigenesis of lactotrophs.
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http://dx.doi.org/10.1007/s00795-008-0411-1 | DOI Listing |
Int J Mol Sci
December 2024
Department of Biological Sciences, University of Delaware, Newark, DE 19716, USA.
The goal of this paper is to discuss the role of ALDH isozymes in different cancers, review advances in ALDH1-targeting cancer therapies, and explore a mechanism that explains how ALDH expression becomes elevated during cancer development. ALDH is often overexpressed in cancer, and each isoform has a unique expression pattern and a distinct role in different cancers. The abnormal expression of ALDHs in different cancer types (breast, colorectal, lung, gastric, cervical, melanoma, prostate, and renal) is presented and correlated with patient prognosis.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Department of Biosciences, Integral University, Lucknow, India.
Introduction: Diabetic retinopathy is a significant microvascular disorder and the leading cause of vision impairment in working-age individuals. Hyperglycemia triggers retinal damage through mechanisms such as the polyol pathway and the accumulation of advanced glycation end products (AGEs). Inhibiting key enzymes in this pathway, aldose reductase (AR) and sorbitol dehydrogenase (SD), alongside preventing AGE formation, may offer therapeutic strategies for diabetic retinopathy and other vascular complications.
View Article and Find Full Text PDFSignal Transduct Target Ther
January 2025
The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia.
Rampant phospholipid peroxidation initiated by iron causes ferroptosis unless this is restrained by cellular defences. Ferroptosis is increasingly implicated in a host of diseases, and unlike other cell death programs the physiological initiation of ferroptosis is conceived to occur not by an endogenous executioner, but by the withdrawal of cellular guardians that otherwise constantly oppose ferroptosis induction. Here, we profile key ferroptotic defence strategies including iron regulation, phospholipid modulation and enzymes and metabolite systems: glutathione reductase (GR), Ferroptosis suppressor protein 1 (FSP1), NAD(P)H Quinone Dehydrogenase 1 (NQO1), Dihydrofolate reductase (DHFR), retinal reductases and retinal dehydrogenases (RDH) and thioredoxin reductases (TR).
View Article and Find Full Text PDFProg Retin Eye Res
December 2024
Department of Ophthalmology, Leiden University Medical Center, Leiden, the Netherlands; Department of Ophthalmology, Amsterdam University Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Retinitis pigmentosa (RP) is a progressive inherited retinal dystrophy, characterized by the degeneration of photoreceptors, presenting as a rod-cone dystrophy. Approximately 20-30% of patients with RP also exhibit extra-ocular manifestations in the context of a syndrome. This manuscript discusses the broad spectrum of syndromes associated with RP, pathogenic mechanisms, clinical manifestations, differential diagnoses, clinical management approaches, and future perspectives.
View Article and Find Full Text PDFJ Biol Chem
December 2024
The Laboratory of Ophthalmology and Vision Science, Department of Ophthalmology, The Joint National Laboratory of Antibody Drug Engineering, Henan Province Engineering Research Center of Fundus Disease and Ocular Trauma Prevention and Treatment, The First Affiliated Hospital of Zhengzhou University, Zhengzhou University, Zhengzhou, China; Henan International Joint Research Laboratory for Ocular Immunology and Retinal Injury Repair, Zhengzhou, China; Kaifeng Key Lab for Cataracts and Myopia, Kaifeng Central Hospital, Kaifeng, China; Eye Institute, Henan Academy of Innovations in Medical Science, Zhengzhou, China. Electronic address:
Genetic mutations in retinol dehydrogenase 5 (RDH5), a rate-limiting enzyme of the visual cycle, is associated with nyctalopia, AMD and stationary congenital fundus albipunctatus (FA). A majority of these mutations impair RDH5 protein expression and intracellular localization. However, the regulatory mechanisms underlying RDH5 metabolism remain unclear.
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