Dataset Information

?(2)-µ-Globulin fragment (a2-f) from kidneys of male rats.

ABSTRACT: The structure of ?(2)-µ-Globulin fragment (A2-f) is not known.?(2)-µ-Globulin fragment (A2-f) is a 15.5 kDa protein that binds equimolar amount of fatty acids in male rat kidneys. The expression of this protein has been shown to change in response to druginduced and genetic hypertension which suggests that it plays an important role in renal fatty acid metabolism under pathological conditions as well as normal conditions. A2-f has sequence homology with amino acid 28-178 of ?(2)-µ-Globulin (A2U) that is synthesized pre-dominantly in the male rat liver and is present in the urine. It is believed that unusual structural features permit A2-f to be targeted to the proximal tubule cell; to escape lysosomal degradation in liver and to enter the cytosol of proximal tubule cells of the kidneys. Homology modeling has been employed to determine the structural elements of this protein and they have been compared with the published structure of A2U. Results suggest differences between the structure of A2-f and its precursor protein A2U.

SUBMITTER: Hai A

PROVIDER: S-EPMC3569602 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

α(2)-µ-Globulin fragment (a2-f) from kidneys of male rats.

Hai Abdul A Kizilbash Nadeem A NA

Bioinformation 20130206 3

The structure of α(2)-µ-Globulin fragment (A2-f) is not known.α(2)-µ-Globulin fragment (A2-f) is a 15.5 kDa protein that binds equimolar amount of fatty acids in male rat kidneys. The expression of this protein has been shown to change in response to druginduced and genetic hypertension which suggests that it plays an important role in renal fatty acid metabolism under pathological conditions as well as normal conditions. A2-f has sequence homology with amino acid 28-178 of α(2)-µ-Globulin (A2U) ...[more]

PMID: 23422892

Similar Datasets

Project description:The brain µ-opioid receptor (MOR) is critical for the analgesic, rewarding, and addictive effects of opioid drugs. However, in rat models of opioid-related behaviors, the circuit mechanisms of MOR-expressing cells are less known because of a lack of genetic tools to selectively manipulate them. We introduce a CRISPR-based Oprm1-Cre knock-in transgenic rat that provides cell type-specific genetic access to MOR-expressing cells. After performing anatomic and behavioral validation experiments, we used the Oprm1-Cre knock-in rats to study the involvement of NAc MOR-expressing cells in heroin self-administration in male and female rats. Using RNAscope, autoradiography, and FISH chain reaction (HCR-FISH), we found no differences in Oprm1 expression in NAc, dorsal striatum, and dorsal hippocampus, or MOR receptor density (except dorsal striatum) or function between Oprm1-Cre knock-in rats and wildtype littermates. HCR-FISH assay showed that iCre is highly coexpressed with Oprm1 (95%-98%). There were no genotype differences in pain responses, morphine analgesia and tolerance, heroin self-administration, and relapse-related behaviors. We used the Cre-dependent vector AAV1-EF1a-Flex-taCasp3-TEVP to lesion NAc MOR-expressing cells. We found that the lesions decreased acquisition of heroin self-administration in male Oprm1-Cre rats and had a stronger inhibitory effect on the effort to self-administer heroin in female Oprm1-Cre rats. The validation of an Oprm1-Cre knock-in rat enables new strategies for understanding the role of MOR-expressing cells in rat models of opioid addiction, pain-related behaviors, and other opioid-mediated functions. Our initial mechanistic study indicates that lesioning NAc MOR-expressing cells had different effects on heroin self-administration in male and female rats.SIGNIFICANCE STATEMENT The brain µ-opioid receptor (MOR) is critical for the analgesic, rewarding, and addictive effects of opioid drugs. However, in rat models of opioid-related behaviors, the circuit mechanisms of MOR-expressing cells are less known because of a lack of genetic tools to selectively manipulate them. We introduce a CRISPR-based Oprm1-Cre knock-in transgenic rat that provides cell type-specific genetic access to brain MOR-expressing cells. After performing anatomical and behavioral validation experiments, we used the Oprm1-Cre knock-in rats to show that lesioning NAc MOR-expressing cells had different effects on heroin self-administration in males and females. The new Oprm1-Cre rats can be used to study the role of brain MOR-expressing cells in animal models of opioid addiction, pain-related behaviors, and other opioid-mediated functions.

Project description:ObjectiveThe current study evaluates the effect of metformin (MET) and /or alpha lipoic acid (ALA) on hypothyroidism and its adverse effects on the cardiac, renal, and, hepatic functions in rats.Materials and methodsRats were divided into five groups: control, rat model of hypothyroidism induced by propylthiouracil (PTU), rat model of hypothyroidism treated with MET, rat model of hypothyroidism treated with ALA, and rat model of hypothyroidism treated with MET and ALA. At the end of the experiment, body weight gain was determined and the blood samples were collected from orbital plexus to measure the serum levels of thyroxine (T4), triiodothyronine (T3) and thyroid stimulating hormone (TSH) by ELISA, glucose level, the activities of lactate dehydrogenase (LDH), creatine kinase MB (CK-MB), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP), and the levels of urea and creatinine spectrophotometrically.ResultsRat model of hypothyroidism revealed a significant decrease in T4 (p < 0.001) and T3 (p < 0.001) and a significant increase in TSH (p < 0.005). This was accompanied by a significant decrease in the body weight gain (p < 0.025) and a significant increase in LDH (p < 0.001), CK-MB (p < 0.001) AST (p < 0.01), ALT (p < 0.016), ALP (p < 0.001), glucose (p < 0.001), urea (p < 0.001) and creatinine (p < 0.001). MET restored T4, T3 and TSH to control values. Treatment with ALA restored T3 and TSH levels. Treatment with Met and /or ALA reduced the levels of glucose, urea and creatinine and the activities of LDH, CK-MB, AST, ALT, and ALP to control-like values. Only ALA improved the reduced body weight gain induced by hypothyroidism.ConclusionThe present findings indicate the ameliorative effects of MET and /or ALA on hypothyroidism and its adverse effects on cardiac, renal and hepatic functions.Graphical abstractSupplementary informationThe online version contains supplementary material available at 10.1007/s40200-022-01063-7.

Dataset Information

?(2)-µ-Globulin fragment (a2-f) from kidneys of male rats.

Publications

α(2)-µ-Globulin fragment (a2-f) from kidneys of male rats.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets