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Loss of T-cell protein tyrosine phosphatase in the intestinal epithelium promotes local inflammation by increasing colonic stem cell proliferation

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Cellular & Molecular Immunology 2018年第4期15卷 367-376页

作者： Stéphanie Bussières-Marmen Valérie Vinette Jeremy Gungabeesoon Isabelle Aubry Luis Alberto Pérez-Quintero Michel L Tremblay department of biochemistry McGill UniversityMontréalQuébecCanada Rosalind and Morris goodman cancer research centre MontréalQuébecCanada department of Microbiology and Immunology McGill UniversityMontréalQuébecCanada

T-cell protein tyrosine phosphatase(TC-PTP)has a critical role in the development of the immune system and has been identified as a negative regulator of ***-nucleotide polymorphisms in the TC-PTP locus have been associated with increased susceptibility to inflammatory bowel diseases(IBDs)in *** further understand how TC-PTP is related to IBDs,we investigated the role of TC-PTP in maintaining the intestinal epithelial barrier using an in vivo genetic *** epithelial cell(IEC)-specific deletion of TC-PTP was achieved in a mouse model at steady state and in the context of dextran sulphate sodium(DSS)-induced ***(KO)of TC-PTP in IECs did not result in an altered intestinal ***,upon DSS treatment,IECspecific TC-PTP KO mice displayed a more severe colitis phenotype with a corresponding increase in the immune response and inflammatory cytokine *** absence of TC-PTP caused an altered turnover of IECs,which is further explained by the role of the tyrosine phosphatase in colonic stem cell(CoSC)*** results suggest a novel role for TC-PTP in regulating the homeostasis of CoSC *** supports the protective function of TC-PTP against IBDs,independently of its previously demonstrated role in intestinal immunity.

关键词： Colonic stem cells DSS-induced colitis intestinal epithelial barrier TC-PTP

Olfactory receptors in neural regeneration in the central nervous system

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Neural Regeneration research 2025年第9期20卷 2480-2494页

作者： Rafael Franco Claudia Garrigós Toni Capó Joan Serrano-Marín Rafael Rivas-Santisteban Jaume Lillo Molecular Neurobiology Laboratory Department of Biochemistry and Molecular BiomedicineFacultat de BiologiaUniversitat de BarcelonaBarcelonaSpain CiberNed Network Center for Biomedical research in Neurodegenerative Diseases Spanish National Health Institute Carlos ⅢMadridSpain School of Chemistry Universitat de BarcelonaBarcelonaSpain department of biochemistry and Physiology School of Pharmacy and Food SciencesUniversitat de BarcelonaBarcelonaSpain Laboratory of Computational Medicine Biostatistics UnitFaculty of MedicineAutonomous University of BarcelonaCampus BellaterraBarcelonaSpain

Olfactory receptors are crucial for detecting odors and play a vital role in our sense of smell,influencing behaviors from food choices to emotional *** receptors also contribute to our perception of flavor and have potential applications in medical diagnostics and environmental *** ability of the olfactory system to regenerate its sensory neurons provides a unique model to study neural regeneration,a phenomenon largely absent in the central nervous *** gained from how olfactory neurons continuously replace themselves and reestablish functional connections can provide strategies to promote similar regenerative processes in the central nervous system,where damage often results in permanent *** the molecular and cellular mechanisms underpinning olfactory neuron regeneration could pave the way for developing therapeutic approaches to treat spinal co rd injuries and neurodegenerative diseases like Alzheimer's *** ctory receptors are found in almost any cell of eve ry orga n/tissue of the mammalian *** ectopic expression provides insights into the chemical structures that can activate olfactory *** addition to odors,olfactory receptors in ectopic expression may respond to endogenous compounds and molecules produced by mucosal colonizing *** analysis of the function of olfactory receptors in ectopic expression provides valuable information on the signaling pathway engaged upon receptor activation and the receptor's role in proliferation and cell differentiation *** review explo res the ectopic expression of olfa ctory receptors and the role they may play in neural regeneration within the central nervous system,with particular attention to compounds that can activate these receptors to initiate regenerative *** suggests that olfactory receptors could serve as potential therapeutic targets for enhancing neural repair and recovery following central nervous syste

关键词： adenosine receptors adrenergic receptors ectopic expression G proteincoupled receptors glia neurons

Epigenetic regulation of the inflammatory response in stroke

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Neural Regeneration research 2025年第11期20卷 3045-3062页

作者： Jingyi Liang Fei Yang Zixiao Li Qian Li School of Basic Medical Sciences Capital Medical UniversityBeijingChina department of Neurobiology School of Basic Medical SciencesCapital Medical UniversityBeijingChina Laboratory for Clinical Medicine Beijing Key Laboratory of Neural Regeneration and RepairCapital Medical UniversityBeijingChina department of Neurology Beijing Tiantan HospitalCapital Medical UniversityBeijingChina China National Clinical research Center for Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina National Center for Healthcare Quality Management in Neurological Diseases Beijing Tiantan HospitalCapital Medical UniversityBeijingChina Chinese Institute for Brain research BeijingChina research Unit of Artificial Intelligence in Cerebrovascular Disease Chinese Academy of Medical SciencesBeijingChina Beijing Engineering research Center of Digital Healthcare for Neurological Diseases BeijingChina department of biochemistry and Molecular Biology School of Basic Medical SciencesCapital Medical UniversityBeijingChina Beijing Key Laboratory of cancer Invasion and Metastasis research Capital Medical UniversityBeijingChina

Stroke is classified as ischemic or hemorrhagic,and there are few effective treatments for either *** mechanisms play a critical role in secondary brain injury following a stroke,which manifests as cytokine release,blood–brain barrier disruption,neuronal cell death,and ultimately behavioral *** the inflammatory response has been shown to mitigate this cascade of events in experimental stroke ***,in clinical trials of anti-inflammatory agents,longterm immunosuppression has not demonstrated significant clinical benefits for *** may be attributable to the dichotomous roles of inflammation in both tissue injury and repair,as well as the complex pathophysiologic inflammatory processes in *** acute harmful inflammatory responses or inducing a phenotypic shift from a pro-inflammatory to an anti-inflammatory state at specific time points after a stroke are alternative and promising therapeutic *** agents that can modulate inflammation requires a detailed understanding of the inflammatory processes of ***,epigenetic reprogramming plays a crucial role in modulating post-stroke inflammation and can potentially be exploited for stroke *** this review,we summarize current findings on the epigenetic regulation of the inflammatory response in stroke,focusing on key signaling pathways including nuclear factor-kappa B,Janus kinase/signal transducer and activator of transcription,and mitogen-activated protein kinase as well as inflammasome *** also discuss promising molecular targets for stroke *** evidence to date indicates that therapeutic targeting of the epigenetic regulation of inflammation can shift the balance from inflammation-induced tissue injury to repair following stroke,leading to improved post-stroke outcomes.

关键词： DNA methylation histone modification intracerebral hemorrhage ischemic stroke neuroinflammation neuroprotection non-coding RNA RNA methylation subarachnoid hemorrhage treatment

Single-cell and spatial omics:exploring hypothalamic heterogeneity

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Neural Regeneration research 2025年第6期20卷 1525-1540页

作者： Muhammad Junaid Eun Jeong Lee Su Bin Lim department of biochemistry&Molecular Biology Ajou University School of MedicineSuwonSouth Korea department of Biomedical Sciences Graduate School of Ajou UniversitySuwonSouth Korea department of Brain Science Ajou University School of MedicineSuwonSouth Korea

Elucidating the complex dynamic cellular organization in the hypothalamus is critical for understanding its role in coordinating fundamental body functions. Over the past decade, single-cell and spatial omics technologies have significantly evolved, overcoming initial technical challenges in capturing and analyzing individual cells. These high-throughput omics technologies now offer a remarkable opportunity to comprehend the complex spatiotemporal patterns of transcriptional diversity and cell-type characteristics across the entire hypothalamus. Current single-cell and single-nucleus RNA sequencing methods comprehensively quantify gene expression by exploring distinct phenotypes across various subregions of the hypothalamus. However, single-cell/single-nucleus RNA sequencing requires isolating the cell/nuclei from the tissue, potentially resulting in the loss of spatial information concerning neuronal networks. Spatial transcriptomics methods, by bypassing the cell dissociation, can elucidate the intricate spatial organization of neural networks through their imaging and sequencing technologies. In this review, we highlight the applicative value of single-cell and spatial transcriptomics in exploring the complex molecular-genetic diversity of hypothalamic cell types, driven by recent high-throughput achievements.

关键词： cellular diversity hypothalamus multi-omics single-cell transcriptomics spatial transcriptomics

Preventive effects of cannabis on neurotoxic and hepatotoxic activities of malathion in rat

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Asian Pacific Journal of Tropical Medicine 2018年第4期11卷 272-279页

作者： Omar M.E.Abdel-Salam Amany A Sleem Eman R Youness Fatma A.Morsy department of Toxicology and Narcotics National Research Centre department of Pharmacology National Research Centre department of Medical biochemistry National Research Centre department of Pathology National Research Centre

Objective: To investigate the effect of Cannabis sativa extract on the development of neuroand hepato-toxicity caused by malathion injection in rats. Methods: The extract of Cannabis sativa was obtained from the plant resin by chloroform treatment. Δ~9-Tetrahydrocannabinol content of the extract(20%) was quantified using gas chromatography–mass spectrometry. The doses of cannabis extract were expressed as Δ~9-tetrahydrocannabinol content of 10 or 20 mg/kg. Malathion(150 mg/kg) was intraperitoneally administered followed after 30 min by the cannabis extract(10 or 20 mg/kg, subcutaneously). Rats were euthanized 4 h later. Malondialdehyde(MDA), reduced glutathione(GSH), nitric oxide and paraoxonase-1(PON-1) activity were determined in brain and liver. Brain 5-lipoxygenase and butyrylcholinesterase(BChE) activity were measured as well. Histopathological examination of brain and liver tissue was also performed. Results: Compared to controls, malathion resulted in increased oxidative stress in brain and liver. MDA and nitric oxide concentrations were significantly increased(P<0.05) and GSH significantly decreased with respect to control levels(P<0.05). Malathion also significantly inhibited PON-1 and BChE activities but had no effect on brain 5-lipoxygenase. Brain MDA concentrations were not altered by cannabis treatment. Cannabis at 20 mg/kg, however, caused significant increase in nitric oxide and restored the GSH and PON-1 activity. Brain BChE activity significantly decreased by 26.1%(P<0.05) after treatment with 10 mg/kg cannabis. Cannabis showed no effect on brain 5-lipoxygenase. On the other hand, rats treated with cannabis exhibited significantly higher levels of liver MDA, nitric oxide and PON-1 activity compared with the malathion control group. Rats treated with only malathion exhibited spongiform changes, neuronal damage in the cerebral cortex and degeneration of some Purkinje cells in the cerebellum. There were also hepatic vacuolar degeneration and dilated an

关键词： Cannabis sativa Malathion Liver damage Brain damage Oxidative stress Paraoxonase 5-Lipoxygenase

Clinical benefits of biochemical markers of bone turnover in Egyptian children with chronic liver diseases

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World Journal of Gastroenterology 2007年第5期13卷 785-790页

作者： Karam A Mahdy Hanaa H Ahmed Fathia Mannaa Azza Abdel-Shaheed Medical biochemistry department National Research Centre Egypt Hormones department National Research Centre Egypt Medical Physiology department National Research Centre Egypt Child Health department National Research Centre Egypt

AIM： To investigate the association between serum insulin-like growth factor 1 （IGF-1）, osteocalcin, and parathyroid hormone （PTH） levels with the etiology and clinical condition of patients with chronic liver disease. METHODS： Eighty children with hepatocellular damage were divided into 3 groups according to the etiology of disease infection： bilharziasis （9 patients）, hepatitis B virus （HBV, 12 patients） and hepatitis C virus （HCV, 29 patients）. The Child score index was found as A in 24 patients, B in 22 patients, C in 4 patients. Thirty healthy children served as control ***, HBcAbIgM, HBcAbIgG, and anti-HCV were detected using ELISA technique. HCV-RNA was measured by reverse transcription polymerase chain reaction （RT-PCR）. Antibllharzial antibodies were detected by indirect haemagglutination test. Liver function tests were performed using autoanalyser. Serum IGF-1, osteocalcin and PTH levels were measured by ELISA technique. Abdominal ultrasonography was also conducted. RESULTS： Serum IGF-1 level was significantly lower in all patient groups with liver diseases, while serum osteocalcin and PTH levels were significantly elevated in patients with HBV and HCV infections compared with the control group. Serum osteocalcin and PTH concentrations were measured with the severity of liver disease from Child A to C. Child A patients unexpectedly showed significantly reduced IGF-1 levels in comparison to patients staged as Child B or C. Serum osteocalcin level was negatively correlated with albumin （14.7 ± 0.54 vs 3.6 ± 0.10, P 〈 0.05）, while that for PTH was positively correlated with total protein （70.1 ± 2.17 vs 6.7 ± 0.10, P 〈 0.05） in patients with HCV infection.

关键词： Liver disease Bone turnover Insulin-like growth factor-1 Osteocalcin Parathyroid hormone

Neuroprotection by misoprostol against rotenone-induced neurotoxicity in rat brain

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Asian Pacific Journal of Tropical Medicine 2018年第1期11卷 40-47页

作者： Omar M.E.Abdel-Salam Amany A Sleem Eman R Youness Nadia A Mohammed Enayat A Omara department of Toxicology and Narcotics National Research Centre department of Pharmacology National Research Centre department of Medical biochemistry National Research Centre department of Pathology National Research Centre

Objective: To investigate the effect of the prostaglandin E1 analogue misoprostol on oxidative stress and neurodegeration caused by subcutaneous rotenone administration in rats. Methods:Rotenone was administered in a dose of 1.5 mg/kg every other day for 2 weeks. Starting from the 1 st day of rotenone injection, rats were subcutaneously treated with misoprostol at doses of10, 100 or 1 000 μg/kg. Rats were evaluated for brain lipid peroxidation(malondialdehyde:MDA), reduced glutathione(GSH), nitric oxide(NO) levels, and paraoxonase-1(PON-1) *** concentrations of the anti-apoptotic protein B cell/lymphoma-2(Bcl-2) were determined in the striatum. Histopathologic examination and the expression of inducible nitric oxide synthase(iNOS) in the cerebral cortex and striatum were also performed. Results: Compared with the vehicle-treated group, rotenone caused a significant increase in brain lipid proxidation(MDA)by 61%(P<0.05) accompanied by an increase in NO by 73.1%(P<0.05) and a decrease in GSH concentration by 29.4%(P<0.05). In addition, brain PON-1 activity significantly decreased by63.0%(P<0.05) and striatal Bcl-2 significantly decreased by 27.9%(P<0.05) with respect to the corresponding control value. Brain sections from rotenone treated rats showed extensive dark pyknotic and apoptotic nuclei in neurons, shrunken cytoplasm and perineuronal *** also caused pronounced expression of iNOS in the cerebral cortex and *** with misoprostol at doses of 100 and 1 000 μg/kg resulted in decreased brain MDA(by 16.5%-23.0%)(P<0.05) and NO levels(by 37.1%-40.7%)(P<0.05) and increased GSH concentrations(by 18.8%-30.1%)(P<0.05). PON-1 activity was significantly increased by80.0%-114.8%(P<0.05) by misoprostol at 100 and 1 000 μg/kg, respectively. In addition,misoprostol treatment restored striatal Bcl-2 concentrations to its normal value. Misoprostol treatment resulted in markedly reduced brain injury and decreased iNOS expression in the cereb

关键词： Misoprostol Rotenone Brain oxidative stress B cell/lymphoma-2 Paraoxonase

Protective and therapeutic potentials of Dunaliella salina on aging-associated cardiac dysfunction in rats

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Asian Pacific Journal of Tropical Biomedicine 2018年第8期8卷 403-410页

作者： Farouk K.El-Baz Gehad A.Abdel Jaleel Dalia O.Saleh Rehab A.Hussein Plant biochemistry department National Research Centre (NRC) Pharmacology department National Research Centre (NRC) Pharmacognosy department National Research Centre (NRC)

Objective: To investigate the possible protective and/or therapeutic potentials of Dunaliella salina(D. salina) biomass, its carotenoid and polar fractions on cardiac dysfunction associated with D-galactose(D-GAL) induced aging in rats. Methods: Aging associated cardiac dysfunction was induced in rats by injection of D-GAL(200 mg/kg; i.p) for 8 weeks. D-GAL injected rats were treated with two regimens; protective regimen where D. salina biomass(250 mg/kg), its carotenoid(250 μg/kg) and polar(250 μg/kg) fractions were given orally for two weeks concurrently with D-GAL injection as well as treatment regimen where the three treatments were given orally for 28 consecutive days after D-GAL injection. Results: D-GAL injection for 8 weeks was accompanied with dramatic electrocardiographic changes as well as profound elevation in serum levels of homocysteine, creatinine kinase isoenzyme and lactate dehydrogenase in addition to the reduction of the cardiac content of glucose trasporter 4. D-GAL also induced reduction in cardiac superoxide dismutase activity and elevation of inducible nitric oxide synthetase and interleukin-6. On the other hand, oral administration of D. salina carotenoid fraction as well as the total biomass significantly attenuated the D-GAL-induced disturbances in the above mentioned parameters where the protective regimen appeared more successful in controlling the manifestations of cardiac dysfunction. The histopathological examination further emphasized the promising results. Besides, the HPLC analysis of the carotenoid fraction of D. salina revealed the presence of 2.31%. salina carotenoid fraction as well as the total biomass amelior β-carotene. Conclusions: Date D-GAL-induced aging associated cardiac dysfunction which is attributed to the potent antioxidant activity of β-carotene.

关键词： Aging Cardiac dysfunction Dunaliella salina Rats

THE ANTISENSE C-HA-RAS OLIGODEOXY-NUCLEOTIDES INHIBIT THE PROLIFERATION OF THE GASTROCARCINOMA-DNA-TRANSFORMED RAT 3-3 CELLS AND REDUCE THE P21 EXPRESSION OF THE CELLS

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Science China Chemistry 1991年第1期34卷 35-41页

作者：许毅邓国仁梁亚云李赤 biochemistry department Beijing Institute for Cancer Research Beijing 100034 PRC

The Rat 3-3 is a secondary transformant of the rat fibroblast cell line (Rat-1) transfectedwith total DNA of a gastrocarcinoma cell line BGC-823. The cells over-express the c-Ha-rasoncogene which contains point mutation at the 12th codon. In order to determine how theactivated c-Ha-ras oncogene expression governs the cell's transformation, two pendadecadeoxy-nucleotides AS-1 and AS-2 were synthesized. AS-1 was complementary to the single strandof the first three codons and the upstream sequence close to the ribosome binding site of c-Ha-ras mRNA. AS-2 was complementary to the 3' end of the first intron and the 5' end ofthe second exon of c-Ha-ras unripe RNA enclosed in the nucleus. The oligonucleotides couldblock either the translation of c-Ha-ras mRNA or the splicing of c-Ha-ras unripe RNA, thusinhibiting the expression of the activated c-Ha-ras oncogene and the proliferation of thetransformed cells Rat 3-3. The inhibitory effect increased with a growing concentration ofthe antisense oligodeoxynucleotide (from 4- 10 μmol/L) and reached its peak at 12 h afterRat 3-3 was treated with AS-1 and AS-2. This effect became weaker afterwards. The p21level, product of c-Ha-ras, in the Rat 3-3, was examined by ELISA method. The resultshows that the amount of p21 in the growth-inhibited cellsis about 30% of that of the controlcells.

关键词： antisense oligodeoxynucleotides transformants inhibition of cell proliferation oncogene