Serum cathelicidin as a marker for diabetic nephropathy in patients with type 1 diabetes

El-Ashmawy, Hazem M.; Ahmed, Azza M.

doi:10.1002/dmrr.3057

Cited by 3 publications

(2 citation statements)

References 32 publications

(60 reference statements)

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“…The antimicrobial peptide cathelicidin (CRAMP in mouse/rat, LL-37 in human) is expressed in many immune cells, such as epithelial cells, and genital cells 10 . CRAMP was initially reported as an immunomodulatory peptide that functions in many autoimmune diseases, such as psoriasis 11 , systemic lupus erythematous 12 , arthritis 13 , atherosclerosis 14 , and type 1 diabetes 15 . Recent studies have identified a role of CRAMP in cardiovascular disease.…”

Section: Introductionmentioning

confidence: 99%

A cathelicidin-related antimicrobial peptide suppresses cardiac hypertrophy induced by pressure overload by regulating IGFR1/PI3K/AKT and TLR9/AMPKα

et al. 2020

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Cathelicidin-related antimicrobial peptide (CRAMP), an antimicrobial peptide, was reported to protect against myocardial ischemia/reperfusion injury. However, the effect of CRAMP on pressure overload-induced cardiac hypertrophy was unknown. This study explored the role of CRAMP on cardiac hypertrophy. A cardiac hypertrophy mouse model was induced by aortic banding surgery. Seven days after surgery, mice were given mCRAMP by intraperitoneal injection (8 mg/kg/d) for 7 weeks. Cardiac hypertrophy was evaluated by the hypertrophic response and fibrosis level as well as cardiac function. Mice were also injected with AAV9-shCRAMP to knockdown CRAMP in the mouse heart. CRAMP levels first increased and then reduced in the remodeling heart, as well as in angiotensin IIstimulated endothelial cells but not in cardiomyocytes and fibroblasts. mCRAMP protected against the pressure overload-induced cardiac remodeling process, while CRAMP knockdown accelerated this process. mCRAMP reduced the inflammatory response and oxidative stress in the hypertrophic heart, while mCRAMP deficiency deteriorated the pressure overload-induced inflammatory response and oxidative stress. mCRAMP inhibited the angiotensin IIstimulated hypertrophic response and oxidative stress in neonatal rat cardiomyocytes, but mCRAMP did not help the angiotensin II-induced inflammatory response and oxidative stress in endothelial cells. Mechanistically, we found that mCRAMP suppressed the cardiac hypertrophic response by activating the IGFR1/PI3K/AKT pathway via directly binding to IGFR1. AKT knockout mice completely reversed the anti-hypertrophic effect of mCRAMP but not its anti-oxidative effect. We also found that mCRAMP ameliorated cardiac oxidative stress by activating the TLR9/AMPKa pathway. This was confirmed by a TLR9 knockout mouse experiment, in which a TLR9 knockout partly reversed the anti-hypertrophic effect of mCRAMP and completely counteracted the anti-oxidative effect of mCRAMP. In summary, mCRAMP protected against pressure overload-induced cardiac hypertrophy by activating both the IGFR1/PI3K/AKT and TLR9/ AMPKa pathways in cardiomyocytes.

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Section: Introductionmentioning

confidence: 99%

A cathelicidin-related antimicrobial peptide suppresses cardiac hypertrophy induced by pressure overload by regulating IGFR1/PI3K/AKT and TLR9/AMPKα

et al. 2020

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“…This finding suggests a considerable short-term induction of CAMP expression and secretion by insulin, glucose, and/or incretins. Of note, CAMP has previously been reported to be linked to diabetes mellitus type 1 [ 25 ], and its circulating levels have been suggested as a marker for diabetic nephropathy [ 26 ]. While a recent study reported decreased CAMP serum concentrations in T2D patients [ 27 ], results from previously published studies are somewhat incongruent with this observation [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Circulating Concentrations of Cathelicidin Anti-Microbial Peptide (CAMP) Are Increased during Oral Glucose Tolerance Test

Höpfinger,

Karrasch,

Schäffler

et al. 2023

IJMS

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Recent investigation has revealed the significant role of Cathelicidin antimicrobial peptide (CAMP) in infection defense and innate immunity processes in adipose tissue. Meanwhile, knowledge of its regulation and functions in metabolic contexts as an adipokine remains sparce. The present study investigated the postprandial regulation of circulating CAMP levels during oral glucose tolerance tests (OGTTs). Eighty-six metabolically healthy volunteers participated in a standardized 75 g-2 h-OGTT setting. The effects of exogenous glucose, insulin, and incretins on CAMP expression in human adipocyte culture (cell-line SGBS) were studied in vitro. CAMP concentrations in blood serum samples were measured by ELISA techniques and adipocyte gene expression levels were quantified by real-time PCR. Of note, base-line CAMP serum quantities were negatively correlated with HDL cholesterol levels as well as with the anti-inflammatory adipokine adiponectin. During the 2 h following glucose ingestion, a significant rise in circulating CAMP concentrations was observed in considerable contrast to reduced quantities of fatty acid binding proteins (FABP) 2 and 4 and dipeptidyl peptidase 4 (DPP4). In SGBS adipocytes, neither differing glucose levels nor insulin or incretin treatment significantly induced CAMP mRNA levels. According to our data, glucose represents a positive postprandial regulator of systemic CAMP. This effect apparently is not mediated by the regulatory impact of glucose metabolism on adipocyte CAMP expression.

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Cathelicidin as a marker for subclinical cardiac changes and microvascular complications in children and adolescents with type 1 diabetes

Matter

Nasef

ShibaAlhamd

et al. 2022

Journal of Pediatric Endocrinology and Metabolism

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Objectives To detect cathelicidin levels in pediatric patients with type 1 diabetes (T1D) as a potential marker for diabetic vascular complications and to assess its relation to diastolic dysfunction as an index for subclinical macrovasculopathy. Methods Totally, 84 patients with T1D were categorized into three groups; newly diagnosed diabetes group (28 patients with a mean age of 12.38 ± 1.99) years, T1D without microvascular complications group (28 patients with a mean age of 13.04 ± 2.27), and T1D with microvascular complications group (28 patients with a mean age of 13.96 ± 2.30). Patients were evaluated using serum cathelicidin levels and echocardiography. Results Total cholesterol, microalbuminuria, and cathelicidin levels were significantly higher in patients with microvascular complications when compared to the other two groups (p<0.001). Additionally, carotid intima-media thickness (CIMT) echocardiography values and diastolic functions were significantly higher in patients with complications (p<0.001). Cathelicidin was positively correlated to the duration of diabetes (r=0.542, p<0.001), total cholesterol (r=0.346, p=0.001), recurrence of hypoglycemia (r=0.351, p=0.001), recurrence of diabetes ketoacidosis (r=0.365, p=0.001), CIMT (r=0.544, p<0.001), and E/A values (r=0.405, p<0.001). Conclusions Serum cathelicidin levels can be used as an early marker for the occurrence and progression of vascular complications in patients with T1D.

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Serum cathelicidin as a marker for diabetic nephropathy in patients with type 1 diabetes

Abstract: Patients with T1DM and DN are characterized by increased serum cathelicidin level. There was an independent relationship between serum cathelicidin level and DN. Serum cathelicidin level can be used as an early marker for the presence and progression of DN in T1DM patients.

Cited by 3 publications

References 32 publications

A cathelicidin-related antimicrobial peptide suppresses cardiac hypertrophy induced by pressure overload by regulating IGFR1/PI3K/AKT and TLR9/AMPKα

A cathelicidin-related antimicrobial peptide suppresses cardiac hypertrophy induced by pressure overload by regulating IGFR1/PI3K/AKT and TLR9/AMPKα

Circulating Concentrations of Cathelicidin Anti-Microbial Peptide (CAMP) Are Increased during Oral Glucose Tolerance Test

Cathelicidin as a marker for subclinical cardiac changes and microvascular complications in children and adolescents with type 1 diabetes

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