Katedra i Zakład Genoterapii Collegium Medicum w Bydgoszczy Uniwersytetu Mikołaja Kopernika w Toruniu.
Published: November 2005
AI Article Synopsis
Article Abstract
Unlabelled: Antisense techniques that inhibit intracellular expression of insulin-like growth factor-I (IGF-I) were efficient in gene therapy of some tumor diseases. IGF-I in the airways is considered to induce lung fibrosis in interstitial lung diseases, inhibit apoptosis of epithelial cells and participate in local carcinogenesis.
Aim Of The Study: The aim of the study was--by examining the IGF-I expression in the lower airways--to evaluate preliminary the efficacy of anti-IGF-I antisense technicques in the treatment of airways diseases.
Material And Methods: The IGF-I expression was examined in the reverse transcriptase--polimerase chain reaction (RT-PCR) applied to A549 human cell line, that is representative for lower airway epithelium and exemplifies the model of bronchioloalveolar adenocarcinoma. IGF-I expression in non-neoplastic lower airways cells was assessed by immunocytochemical staining (anti-IGF-I) in cytological materials originating from bronchoalveolar lavage (BAL) of sarcoidosis and asbestosis patients and in individuals free of lung pathology.
Results: The IGF-I expression was detected in A549 cells with use of RT-PCR method (3 independent probes). In BAL cytological specimens the appearance of IGF-I was found, mainly in alveolar macrophages (62 +/- 6, 5 in sarcoidosis vs. 36 +/- 6 in controls, p=0,09), as well as in BAL lymphocytes.
Conclusions: Summing up, the antisense technicques, blocking the intracellular IGF-I expression may be potentially useful in treatment of selected lower airways, both tumor (non-small cell lung carcinoma) and non-tumor (ILD complicated with lung fibrosis) conditions.
Despite their pivotal role, the evolutionary origins of vertebrate digestive systems remain enigmatic. We explored the cellular characteristics of the amphioxus () digestive tract, a model for the presumed primitive chordate digestive system, using bulk tissue companioned with single-cell RNA sequencing. Our findings reveal segmentation and a rich diversity of cell clusters, and we highlight the presence of epithelial-like, ciliated cells in the amphioxus midgut and describe three types of endocrine-like cells that secrete insulin-like, glucagon-like, and somatostatin-like peptides.
Senile osteoporosis (SOP) is a multifactorial, age-related progressive phenomenon with a considerable morbidity and mortality. IGF-1 is an important regulator of bone reconstruction and metabolism throughout life. Nevertheless, our previous study unexpectedly found there is no change in the peak bone mass with a altered IGF-1 gene expression leaded by IGF-1 c.
Context: In most cases of non-islet cell tumor hypoglycemia (NICTH), high molecular weight forms of insulin-like growth factor II, commonly referred to as big IGF-II, cause hypoglycemia. MicroRNA-483 (miR-483), encoded within an intron of IGF2 gene, has been suggested to be co-expressed with IGF-II.
Objective: The aim of this study is to demonstrate the utility and reliability of circulating miR-483 as a biomarker for diagnosis and therapeutic outcome of NICTH.
Fish oocyte maturation (FOM) is a critical biological process that occurs before ovulation and is influenced by gonadotropins, particularly luteinizing hormone (LH). The release of LH stimulates the ovarian follicle to produce a maturation-inducing hormone (MIH), specifically 17α, 20β-dihydroxy-4-pregnen-3-one (17α, 20β-DP), which initiates the formation of maturation-promoting factor (MPF) through the activation of cyclin B and cdc2 kinase. Insulin-like growth factor I (IGF-I) significantly regulates ovarian functions, including steroidogenesis, by activating its membrane receptors and the tyrosine kinase pathway.
Women with intrahepatic cholestasis of pregnancy (ICP) have hypercholanemia alongside an increased risk of dyslipidemia. We investigated how cholic acid (CA) supplementation in murine pregnancy impacts adipose tissue function. Mice were fed normal or 0.
