Dataset Information

1?,25-dihydroxyvitamin D₃-eluting nanofibrous dressings induce endogenous antimicrobial peptide expression.

ABSTRACT:

Aim

The aim of this study was to develop a nanofiber-based dressing capable of local sustained delivery of 1?,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) and augmenting human CAMP induction.

Materials & methods

Nanofibrous wound dressings containing 1,25(OH)₂D₃ were successfully prepared by electrospinning, which were examined in vitro, in vivo and ex vivo.

Results

1,25(OH)₂D₃ was successfully loaded into nanofibers with encapsulation efficiency larger than 90%. 1,25(OH)₂D₃ showed a sustained release from nanofibers over 4 weeks. Treatment of U937 and HaCaT cells with 1,25(OH)₂D₃-loaded poly(?-caprolactone) nanofibers significantly induced hCAP18/LL37 expression in monocytes and keratinocytes, skin wounds of humanized transgenic mice and artificial wounds of human skin explants.

Conclusion

1,25(OH)₂D₃ containing nanofibrous dressings could enhance innate immunity by inducing antimicrobial peptide production.

SUBMITTER: Jiang J

PROVIDER: S-EPMC6219435 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Publications

1α,25-dihydroxyvitamin D<sub>3</sub>-eluting nanofibrous dressings induce endogenous antimicrobial peptide expression.

Jiang Jiang J Zhang Yang Y Indra Arup K AK Ganguli-Indra Gitali G Le Mai N MN Wang Hongjun H Hollins Ronald R RR Reilly Debra A DA Carlson Mark A MA Gallo Richard L RL Gombart Adrian F AF Xie Jingwei J

Nanomedicine (London, England) 20180601 12

<h4>Aim</h4>The aim of this study was to develop a nanofiber-based dressing capable of local sustained delivery of 1α,25-dihydroxyvitamin D<sub>3</sub> (1,25(OH)<sub>2</sub>D<sub>3</sub>) and augmenting human CAMP induction.<h4>Materials & methods</h4>Nanofibrous wound dressings containing 1,25(OH)<sub>2</sub>D<sub>3</sub> were successfully prepared by electrospinning, which were examined in vitro, in vivo and ex vivo.<h4>Results</h4>1,25(OH)<sub>2</sub>D<sub>3</sub> was successfully loaded into ...[more]

PMID: 29972648

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Project description:BackgroundGlaucoma is an optic neuropathy characterized by loss of function and death of retinal ganglion cells (RGCs), leading to irreversible vision loss. Neuroinflammation is recognized as one of the causes of glaucoma, and currently no treatment is addressing this mechanism. We aimed to investigate the anti-inflammatory and neuroprotective effects of 1,25(OH)2D3 (1α,25-dihydroxyvitamin D3, calcitriol), in a genetic model of age-related glaucomatous neurodegeneration (DBA/2J mice).MethodsDBA/2J mice were randomized to 1,25(OH)2D3 or vehicle treatment groups. Pattern electroretinogram, flash electroretinogram, and intraocular pressure were recorded weekly. Immunostaining for RBPMS, Iba-1, and GFAP was carried out on retinal flat mounts to assess retinal ganglion cell density and quantify microglial and astrocyte activation, respectively. Molecular biology analyses were carried out to evaluate retinal expression of pro-inflammatory cytokines, pNFκB-p65, and neuroprotective factors. Investigators that analysed the data were blind to experimental groups, which were unveiled after graph design and statistical analysis, that were carried out with GraphPad Prism. Several statistical tests and approaches were used: the generalized estimated equations (GEE) analysis, t-test, and one-way ANOVA.ResultsDBA/2J mice treated with 1,25(OH)2D3 for 5 weeks showed improved PERG and FERG amplitudes and reduced RGCs death, compared to vehicle-treated age-matched controls. 1,25(OH)2D3 treatment decreased microglial and astrocyte activation, as well as expression of inflammatory cytokines and pNF-κB-p65 (p < 0.05). Moreover, 1,25(OH)2D3-treated DBA/2J mice displayed increased mRNA levels of neuroprotective factors (p < 0.05), such as BDNF.Conclusions1,25(OH)2D3 protected RGCs preserving retinal function, reducing inflammatory cytokines, and increasing expression of neuroprotective factors. Therefore, 1,25(OH)2D3 could attenuate the retinal damage in glaucomatous patients and warrants further clinical evaluation for the treatment of optic neuropathies.

Project description:Percutaneous transluminal angioplasty (PTA) of stenotic arteriovenous fistulas (AVFs) is performed to maintain optimal function and patency. The one-year patency rate is 60% because of venous neointimal hyperplasia (VNH) and venous stenosis (VS) formation. Immediate early response gene X-1 (Iex-1) also known as Ier3 increases in response to wall shear stress (WSS), and can cause VNH/VS formation in murine AVF. In human stenotic samples from AVFs, we demonstrated increased gene expression of Ier3. We hypothesized that 1α, 25-dihydroxyvitamin D3, an inhibitor of IER3 delivered as 1α, 25-dihydroxyvitamin D3 encapsulated in poly lactic-co-glycolic acid (PLGA) nanoparticles loaded in Pluronic F127 hydrogel (1,25 NP) to the adventitia of the stenotic outflow vein after PTA would decrease VNH/VS formation by reducing Ier3 and chemokine (C-C motif) ligand 2 (Ccl2) expression. In our murine model of AVF stenosis treated with PTA, increased expression of Ier3 and Ccl2 was observed. Using this model, PTA was performed and 10-μL of 1,25 NP or control vehicle (PLGA in hydrogel) was administered by adventitial delivery. Animals were sacrificed at day 3 for unbiased whole genome transcriptomic analysis and at day 21 for immunohistochemical analysis. Doppler US was performed weekly after AVF creation. At day 3, significantly lower gene expression of Ier3 and Ccl2 was noted in 1,25 NP treated vessels. Twenty-one days after PTA, 1,25 NP treated vessels had increased lumen vessel area, with decreased neointima area/media area ratio and cell density compared to vehicle controls. There was a significant increase in apoptosis, with a reduction in CD68, F4/80, CD45, pro-inflammatory macrophages, fibroblasts, Picrosirius red, Masson's trichrome, collagen IV, and proliferation accompanied with higher wall shear stress (WSS) and average peak velocity. IER3 staining was localized to CD68 and FSP-1 (+) cells. After 1,25 NP delivery, there was a decrease in the proliferation of α-SMA (+) and CD68 (+) cells with increase in the apoptosis of FSP-1 (+) and CD68 (+) cells compared to vehicle controls. RNA sequencing revealed a decrease in inflammatory and apoptosis pathways following 1,25 NP delivery. These data suggest that adventitial delivery of 1,25 NP reduces VNH and venous stenosis formation after PTA.

Dataset Information

1?,25-dihydroxyvitamin D₃-eluting nanofibrous dressings induce endogenous antimicrobial peptide expression.

Aim

Materials & methods

Results

Conclusion

Publications

1α,25-dihydroxyvitamin D<sub>3</sub>-eluting nanofibrous dressings induce endogenous antimicrobial peptide expression.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

Dataset Information

1?,25-dihydroxyvitamin D3-eluting nanofibrous dressings induce endogenous antimicrobial peptide expression.

Aim

Materials & methods

Results

Conclusion

Publications

1α,25-dihydroxyvitamin D<sub>3</sub>-eluting nanofibrous dressings induce endogenous antimicrobial peptide expression.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

1?,25-dihydroxyvitamin D₃-eluting nanofibrous dressings induce endogenous antimicrobial peptide expression.