The streptozotocin-induced rat model of diabetes mellitus evidences significant reduction of myosin-Va expression in the brain

Costa, Alice Vieira da; Calábria, Luciana Karen; Nascimento, Rafael; Carvalho, Wender Santana; Goulart, Luiz Ricardo; Espindola, Foued Salmen

doi:10.1007/s11011-011-9259-5

Cited by 12 publications

(14 citation statements)

References 29 publications

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“…Myosin-IIB modulates neurotransmitter release from synapses [83] while myosin-Va mediates synaptic vesicle trafficking [84]. We recently demonstrated that acute diabetes (20 days) alters protein and mRNA expression of myosin-IIB and myosin-Va in the rat brains [21, 23]. In the present study, we revealed an increased protein and mRNA expression of myosin-IIB and a decreased one of myosin-Va in chronic diabetic rat brains (90 days).…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, we revealed an increased protein and mRNA expression of myosin-IIB and a decreased one of myosin-Va in chronic diabetic rat brains (90 days). It is possible that these translational and transcriptional changes are due to low insulin level and high glucose level in circulation providing a possible dysfunction in vesicle/organelle movement [21, 23]. …”

Section: Discussionmentioning

confidence: 99%

“…In spite of the recent studies that have shown relationship between diabetes and the expression of molecular motors, as myosin-IIB [21], myosin heavy-chain [29], myosin-Va [23, 25], and myosin-IXB [30], the pathways linked among myosin expression, oxidative stress, and diabetes mellitus are still unclear. The present study aimed to evaluate the effect of the use of antioxidant supplementation on myosins expression in brain of chronic streptozotocin-induced diabetes experimental rat model.…”

Section: Introductionmentioning

confidence: 99%

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Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains

et al. 2013

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Diabetes mellitus is a disease characterized by persistent hyperglycemia, which may lead to brain tissue damage due to oxidative stress and also contributes to neuronal death and changes in synaptic transmission. This study evaluated the effect of oxidative stress and the use of antioxidants supplementation on myosins expression levels in the brains of chronic diabetic rats induced by streptozotocin. Lipid peroxidation, antioxidant enzymes activities, and myosins-IIB and -Va expressions at transcriptional and translational levels were examined after 90 days induction. The chronic effect of the diabetes led to the upregulation of superoxide dismutase (SOD) and catalase (CAT) activities, and the downregulation of glutathione peroxidase (GPx), but there was no statistically significant increase in the malondialdehyde (MDA) levels. These alterations were accompanied by high myosin-IIB and low myosin-Va expressions. Although the antioxidant supplementation did not interfere on MDA levels, the oxidative stress caused by chronic hyperglycemia was reduced by increasing SOD and restoring CAT and GPx activities. Interestingly, after supplementation, diabetic rats recovered only myosin-Va protein levels, without interfering on myosins mRNA levels expressed in diabetic rat brains. Our results suggest that antioxidant supplementation reduces oxidative stress and also regulates the myosins protein expression, which should be beneficial to individuals with diabetes/chronic hyperglycemia.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains

et al. 2013

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“…injection of 10% chloral hydrate (500 mg/kg) at day 1, 3, 7, 14 and 30 following-SE induction. Following decapitation, the brain was removed as previously described (17) for RNA isolation. Total RNA was extracted with TRIzol reagent (Gibco; Thermo Fisher Scientific, Inc., Waltham, MA, USA) and both the concentration and the purity of RNA were then determined at 260/280 nm using a NanoDrop spectrophotometer.…”

Section: Animalsmentioning

confidence: 99%

Antagonist targeting microRNA-146a protects against lithium-pilocarpine-induced status epilepticus in rats by nuclear factor-κB pathway

Wang

2018

Mol Med Report

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Previous studies have indicated that nuclear factor-κB (NF-κB) has an important role in the pathogenesis of epilepsy. The aim of the present study was to evaluate the expression of microRNA (miRNA)‑146a, phosphorylated (p)‑P65/P65, B‑cell lymphoma‑2(Bcl‑2)/Bcl‑2‑associated X protein (Bax) and pro‑inflammatory cytokines, such as interleukin (IL)‑6, IL‑1β and tumor necrosis factor (TNF‑α) in the brain tissue of rats with epilepsy. Sprague‑Dawley rats were used to establish the epilepsy model using the lithium‑pilocarpine method. The expression of miR‑146a, pro‑inflammatory cytokines, P‑glycoprotein (P‑gp), Bcl‑2/Bax and p‑P65/P65 were assessed by reverse transcription‑semi‑quantitative polymerase chain reaction, enzyme‑linked immunosorbent assay and western blotting, respectively. Hematoxylin and eosin staining was used to determine the pathology of epilepsy. The current findings revealed that the expression of miR‑146a was greater in the model group compared with the control group, and that the expression of miR‑146a reached a maximum at 7 days post‑treatment. The expression levels of IL‑1β, IL‑6 and TNF‑α were significantly reduced in the miR‑146a antagonist group when compared with the model group. Additionally, the expression levels of P‑gp and p‑P65/P65 were significantly reduced following the addition of the miR‑146a antagonist, whereas the expression levels of Bcl‑2/Bax significantly increased under the same conditions. Therefore, the NF‑κB pathway and miR‑146a may be potential therapeutic targets in the treatment of epilepsy.

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“…Similarly, nNOS uncoupling has been shown to be responsible for dysfunctional nitrergic vasorelaxation of penile arteries from insulin-resistant obese Zucker rats [10]. Recently, expression of myosin Va has been reported to be reduced in neuronal tissues from the brain of animal models of diabetes mellitus [33]. Thus it is interesting to speculate that myosin Va defects may contribute to the pathogenesis of diabetic gastroparesis and erectile dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Myosin Va Plays a Role in Nitrergic Smooth Muscle Relaxation in Gastric Fundus and Corpora Cavernosa of Penis

et al. 2014

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The intracellular motor protein myosin Va is involved in nitrergic neurotransmission possibly by trafficking of neuronal nitric oxide synthase (nNOS) within the nerve terminals. In this study, we examined the role of myosin Va in the stomach and penis, proto-typical smooth muscle organs in which nitric oxide (NO) mediated relaxation is critical for function. We used confocal microscopy and co-immunoprecipitation of tissue from the gastric fundus (GF) and penile corpus cavernosum (CCP) to localize myosin Va with nNOS and demonstrate their molecular interaction. We utilized in vitro mechanical studies to test whether smooth muscle relaxations during nitrergic neuromuscular neurotransmission is altered in DBA (dilute, brown, non-agouti) mice which lack functional myosin Va. Myosin Va was localized in nNOS-positive nerve terminals and was co-immunoprecipitated with nNOS in both GF and CCP. In comparison to C57BL/6J wild type (WT) mice, electrical field stimulation (EFS) of precontracted smooth muscles of GF and CCP from DBA animals showed significant impairment of nitrergic relaxation. An NO donor, Sodium nitroprusside (SNP), caused comparable levels of relaxation in smooth muscles of WT and DBA mice. These normal postjunctional responses to SNP in DBA tissues suggest that impairment of smooth muscle relaxation resulted from inhibition of NO synthesis in prejunctional nerve terminals. Our results suggest that normal physiological processes of relaxation of gastric and cavernosal smooth muscles that facilitate food accommodation and penile erection, respectively, may be disrupted under conditions of myosin Va deficiency, resulting in complications like gastroparesis and erectile dysfunction.

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The streptozotocin-induced rat model of diabetes mellitus evidences significant reduction of myosin-Va expression in the brain

Cited by 12 publications

References 29 publications

Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains

Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains

Antagonist targeting microRNA-146a protects against lithium-pilocarpine-induced status epilepticus in rats by nuclear factor-κB pathway

Myosin Va Plays a Role in Nitrergic Smooth Muscle Relaxation in Gastric Fundus and Corpora Cavernosa of Penis

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