Interaction between fragile histamine triad and protein kinase C alpha in human non-small cell lung cancer tissues

Objective To investigate the interaction between fragile histamine triad (FHIT) and protein kinase C alpha (PKCα) in human non-small cell lung cancer tissues. Methods FHIT and PKCα double positive samples were screened by immunohistochemical staining from 13 human non-small cell lung cancer tissues. Co-immunoprecipitation was performed by using anti-FHIT and anti-PKCα. The immune precipitate was analyzed by SDS-PAGE and Western blot. Results Immune precipitate staining detection showed that 3 samples out of the 13 cases were double positive for FHIT and PKCα. FHIT protein was present in the immune precipitate of anti-PKCα while there was PKCα in the immune precipitate of anti-FHITmAb. Conclusion FHIT and PKCα exist as a complex in human non-small cell lung cancer tissues, which will provide a new route for studying the pathogenesis and immunotherapy of human non-small cell lung cancer.

Effect of Combination Regimen of Low-dose Gossypol Acetic Acid with Steroid Hormones on Expression of Protein Kinase C alpha (PKC-α) and Cyclin D1 in Rat Testes

Objective To investigate the contraceptive mechanism of combination regimen of low- dose gossypol acetic acid （GA） with steroid hormones [desogestre/ethinylestradiol/ testosterone undeeanote（DSG/EE/TU）]. Methods Adult male rats were randomly divided into four groups. Group GH： rats were fed orally with gossypol acetic acid （GA, 12.5 mg/kg） and desogestrel （DSG, 0.125 mg/kg）/ ethinylestradiol （EE, 0.025 mg/kg）/testosterone undecanoate （TU, 100 mg/kg per day, qd X4 weeks or 10 weeks）; group G： a single dose of GA （12.5 mg/kg per day, qd X 4 weeks or I0 weeks）; group H： the same dosage of DSG/EE/TUas in group GH; group C： rats were treated with vehicle （1% methyl cellulose） as the control. Expression of protein kinase C alpha （PKC-a） and cyclin D1 in rat testes were tested mainly by immunohistochemistry （IHC） and Western blotting. Results IHC results showed that protein PKC- a was expressed mainly in interstitial tissue of testis among seminiferous tubule. The expression of PKC-oc in groups H and GH at week 10 was decreased greatly compared with that in group C. The protein cyclin D1 was expressed mainly in residual body of seminiferous tubule eavosurface and interstitial tissue among seminiferous tubule of testis. Western blotting results showed that the expression of PKC-a in groups H and GH at week 10 was decreased significantly compared with that in group C （P〈0.05）. The expression of cyclin D1 in groups G, H or GH at week 10 rose significantly compared with that in group C （P 〈0.05）.Conclusion The administration of low-dose gossypol acetic acid with steroid hormones for 10 weeks can decrease the expression of PKC-a greatly.

Adipose mesenchymal stem cell-derived extracellular vesicles reduce glutamate-induced excitotoxicity in the retina

Adipose mesenchymal stem cells(ADSCs)have protective effects against glutamate-induced excitotoxicity,but ADSCs are limited in use for treatment of optic nerve injury.Studies have shown that the extracellular vesicles(EVs)secreted by ADSCs(ADSC-EVs)not only have the function of ADSCs,but also have unique advantages including non-immunogenicity,low probability of abnormal growth,and easy access to target cells.In the present study,we showed that intravitreal injection of ADSC-EVs substantially reduced glutamate-induced damage to retinal morphology and electroretinography.In addition,R28 cell pretreatment with ADSC-EVs before injury inhibited glutamate-induced overload of intracellular calcium,downregulation ofα-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptor(AMPAR)subunit GluA2,and phosphorylation of GluA2 and protein kinase C alpha in vitro.A protein kinase C alpha agonist,12-O-tetradecanoylphorbol 13-acetate,inhibited the neuroprotective effects of ADSC-EVs on glutamate-induced R28 cells.These findings suggest that ADSCEVs ameliorate glutamate-induced excitotoxicity in the retina through inhibiting protein kinase C alpha activation.