Cigarette smoke inhalation aggravates diabetic kidney injury in rats

Jiang, Songling; Quan, Van; Sung, Jae Hyuck; Lee, Moo-Yeol; Ha, Hunjoo

doi:10.1039/c9tx00201d

Cited by 13 publications

(9 citation statements)

References 54 publications

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“…Our studies have demonstrated that Nicotine and high glucose-mediated oxidative stress contributed to kidney cell injury (Lan, et al 2016;Jiang, et al 2019;Wen, et al 2019). NADPH oxidases (Nox) is a membrane-bound enzyme complex to generate superoxide, a substrate for subsequent reactions to cause R.O.S.…”

Section: Discussionmentioning

confidence: 93%

“…Smoking has been reported to be an important risk factor for diabetes, and smokers have twice the risk of developing diabetes as non-smokers (Mardarowicz, et al 2010). Animal experiments have also con rmed that cigarette smoking aggravates diabetic kidney injury in rats and mice (Jiang, et al 2019;Jaimes, et al 2021). Recent studies demonstrate that Nicotine, one of the highly active compounds in cigarette smoke, contributes to the pathogenesis of smokingmediated kidney dysfunction (Hukkanen, et al 2005;Rezonzew, et al 2012).…”

Section: Introductionmentioning

confidence: 98%

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Nicotine exacerbates diabetic nephropathy through upregulation of Grem1 expression

Chen

Xiao

Xue

et al. 2022

Preprint

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Background Diabetic nephropathy (DN) is a major complication of diabetes mellitus. The tobacco epidemic exacerbates kidney damage in patients with DN. Clinical reports indicate that smoking is a significant risk factor for chronic kidney disease, including DN; however, the underlying molecular mechanisms remain unclear. Method In the present study, we used a diabetic mouse model to investigate the molecular mechanisms for nicotine-exacerbated DN. Twelve-week-old female mice were injected with streptozotocin (STZ) to establish a hyperglycemic diabetic model. After four months, the control and hyperglycemic diabetic mice were further divided into four groups (control, Nicotine, diabetic, Nicotine + diabetic) by intraperitoneal injection of Nicotine or PBS. After another two months, urine and blood were collected for kidney injury assay, and renal tissues were harvested for further molecular assays using RNA-seq analysis, real-time PCR, Western blot, and immunohistochemistry. In in vitro studies, we used siRNA to suppress Grem1 expression in human podocytes and then treated them with Nicotine and high glucose to compare podocyte injury. Result Nicotine administration alone did not cause apparent kidney injury, but it significantly increased hyperglycemia-induced albuminuria, BUN, and the expression of KIM-1 and NGAL. Results from RNA-seq analysis, real-time PCR, and western blot analysis revealed that, compared to hyperglycemia or Nicotine alone, the combination of nicotine treatment and hyperglycemia significantly increased the expression of Grem1 and activated the TGF-β pathway. In vitro experiments, suppression of Grem1 expression attenuated nicotine-exacerbated podocyte injury. Conclusion Grem1 plays a vital role in the nicotine-exacerbated DN. Grem1 may be a potential therapeutic target for chronic smokers with DN.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 98%

Nicotine exacerbates diabetic nephropathy through upregulation of Grem1 expression

Chen

Xiao

Xue

et al. 2022

Preprint

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“…Many studies have shown that there is a relationship between smoking and chronic kidney disease. CS could accelerate oxidative stress and increase the production of reactive oxygen species to induce chronic kidney disease 51 , 52 . In this study, the effects of EC and CS exposure on the kidneys of mice has also been evaluated, and the effect of CS on the kidney index was greater than that of EC.…”

Section: Discussionmentioning

confidence: 99%

The toxic effects of electronic cigarette aerosol and cigarette smoke on cardiovascular, gastrointestinal and renal systems in mice

Xu,

Duan,

Yang

et al. 2023

Sci Rep

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Electronic cigarette (EC) has been suggested to be less harmful than cigarette smoking, but the research on the full extent of their harm reduction potential is still lacking. This study aimed to evaluate the influence of EC aerosol and cigarette smoke (CS) on cardiovascular, gastrointestinal, and renal functions in mice after prolonged exposure. Forty-eight C57BL/6J male mice were randomly grouped and then exposed to fresh air (control), mung bean-flavored EC aerosol with low and high dose (EC1L, 6 mg/kg; EC1H, 12 mg/kg), watermelon-flavored EC aerosol with low and high dose (EC2L, 6 mg/kg; EC2H, 12 mg/kg), and finally a cigarette smoke (CS, 6 mg/kg), respectively. After 10 weeks of exposure, the heart rate increased for both the EC and CS groups, and the effect of CS on blood oxygen saturation was significantly higher than that of the EC group (P < 0.01). Proteomic analysis of the heart tissue showed that the overlapped differential expression protein from the EC and CS exposures was Crip2. For the gastrointestinal system, oral mucosa was significantly damaged in CS group. Compare with CS, EC had significantly fewer negative effects on most of the indictors which focused on in this study.

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“…Vascular inflammation and oxidative stress are implicated as essential factors in the pathogenesis and progression of COPD. 18 , 19 Previous studies have reported that cigarette smoke exposure may induce redox imbalance by shifting the balance between oxidants and antioxidants. 20 The airway epithelium is the first protective barrier between the pulmonary tissues and air, making it extremely susceptible to the stimulation of harmful substances, such as PM2.5 and smoke.…”

Section: Discussionmentioning

confidence: 99%

Identification of Small Airway Epithelium-Related Hub Genes in Chronic Obstructive Pulmonary Disease

Lin¹,

Lin²,

Chen³

et al. 2022

COPD

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Background Pulmonary small airway epithelia are the primary site of cellular and histological alterations in chronic obstructive pulmonary disease (COPD), while the potential therapeutic hub genes of pulmonary epithelia are rarely identified to elucidate profound alterations in the progression of the disease. Methods Microarray dataset of GSE11906 containing small airway epithelia from 34 healthy non-smokers and 33 COPD patients was applied to screen differentially expressed genes (DEGs). Weighted gene correlation network analysis (WGCNA) was further used to identify the hub genes related to clinical features. Moreover, single-cell RNA sequencing data from GSE173896 and GSE167295 dataset were applied to explore the expression and distribution of the hub genes. The expression levels of hub genes in epithelial cells stimulated by cigarette smoke extract (CSE) were detected by RT-qPCR. Results Ninety-eight DEGs correlated with clinical features of COPD were identified via limma and WGCNA. Eight hub genes (including AKR1C3 , ALDH3A1 , AKR1C1 , CYP1A1 , GPX2 , CBR3 , AKR1B1 and GSR ) that might exert an antioxidant role in COPD process were identified. Single-cell transcriptomic analysis indicated that the expressions of AKRAC3 , ALDH3A1 , GPX2 , CBR3 and AKR1B1 were significantly increased in the COPD group when compared with the normal group. Moreover, we found that the expression of ALDH3A1 was the most abundantly expressed in ciliated cells. RT-qPCR results indicated that the majority of candidate novel genes were significantly elevated when the epithelial cells were exposed to CSE. Conclusion Through integrating limma, WGCNA, and protein-protein interaction (PPI) analysis, a total of eight candidate hub genes of pulmonary airway epithelia were identified in COPD. Moreover, single-cell transcriptomic analysis indicated that ALDH3A1 was enriched in ciliated cells, which may provide a new insight into the pathogenesis and treatment of COPD.

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Cigarette smoke inhalation aggravates diabetic kidney injury in rats

Cited by 13 publications

References 54 publications

Nicotine exacerbates diabetic nephropathy through upregulation of Grem1 expression

Nicotine exacerbates diabetic nephropathy through upregulation of Grem1 expression

The toxic effects of electronic cigarette aerosol and cigarette smoke on cardiovascular, gastrointestinal and renal systems in mice

Identification of Small Airway Epithelium-Related Hub Genes in Chronic Obstructive Pulmonary Disease

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