Background: Netrin-1 is a diagnostic biomarker that has been identified recently for chronic renal failure (CRF) in animal experiments. Netrin-1 levels in urine have been shown to have increased significantly at the acute kidney damage. Human studies on the relation between the CRF and plasma netrin-1 levels have not been found in the literature. This study aimed to investigate whether plasma netrin-1 levels increased in the early stages of the CRF in diabetic patients.
Methods: Plasma samples from healthy volunteers and diabetic patients with and without microalbuminuria were collected after receiving consent. Netrin-1 in plasma was quantified by enzyme-linked immunosorbent assay and the data were analyzed to determine whether plasma netrin-1 correlates significantly with disease progression.
Result: Plasma netrin-1 level in microalbuminuric diabetic patients was significantly higher than in normoalbuminuric diabetic patients and the control group. However, no significant difference between normoalbuminuric patients and control group was determined. Plasma netrin-1 level was significantly associated with albuminuria and estimated glomerular filtration rate, independently of age and sex.
Conclusion: This study supports that plasma netrin-1 level increases significantly when glomerular damage occurs in diabetic nephropathy.
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http://dx.doi.org/10.1002/jcla.21965 | DOI Listing |
Introduction: Understanding the molecular signals associated with the progression of kidney disease is vital for risk stratification and targeted treatment. Recent advances in RNA-sequencing technique has enabled us to characterize extracellular transcriptome profiles for precision diagnostics.
Method: We evaluated the plasma mRNA profile of participants exhibiting slow (n=119) and fast (n=119) decline in estimated glomerular filtration rate (eGFR) among the Chronic Renal Insufficiency Cohort (CRIC) in a nested case control study.
bioRxiv
November 2024
Department of Cell Biology and Physiology, School of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.
The kidney vasculature has a complex arrangement, which runs in both series and parallel to perfuse the renal tissue and appropriately filter plasma. Recent studies have demonstrated that the development of this vascular pattern is dependent on netrin-1 secreted by renal stromal progenitors. Mice lacking netrin-1 develop an arterial tree with stochastic branching, particularly of the large interlobar vessels.
View Article and Find Full Text PDFCNS Neurosci Ther
September 2024
Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Background: Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by dopaminergic neuron degeneration and diverse motor and nonmotor symptoms. Early diagnosis and intervention are crucial but challenging due to reliance on clinical presentation. Recent research suggests potential biomarkers for early detection, including plasma netrin-1 (NTN-1), a protein implicated in neuronal survival.
View Article and Find Full Text PDFThe guidance cue netrin-1 promotes both growth cone attraction and growth cone repulsion. How netrin-1 elicits these diverse axonal responses, beyond engaging the attractive receptor DCC and repulsive receptors of the UNC5 family, remains elusive. Here we demonstrate that murine netrin-1 induces biphasic axonal responses in cortical neurons: attraction at lower concentrations and repulsion at higher concentrations using both a microfluidic-based netrin-1 gradient and bath application of netrin-1.
View Article and Find Full Text PDFBiomedicines
March 2024
Department of Human Neurosciences, Sapienza University, 00185 Rome, Italy.
Background: Ischemic stroke may trigger neuroplastic changes via proliferation, migration towards the lesion, and differentiation of neuroprogenitor cells into mature neurons. Repetitive Transcranial Magnetic Stimulation (rTMS) may promote brain plasticity. This study aimed to assess rTMS's effect on post-stroke endogenous neuroplasticity by dosing plasma miRs 17~92, Netrin-1, Sema3A, and BDNF.
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