Microvascular research · 2026
UVB-induced cutaneous microvascular responses and NOS-related modulation assessed by multimodal in vivo imaging and graph-based OCTA analysis.
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Shin Paul, Jeong Seungpil, Choi Yean Jung
Аннотация
BACKGROUND: Ultraviolet B (UVB) irradiation induces inflammatory and vascular alterations in the skin, including changes in microvascular perfusion and endothelial activation. However, quantitative in vivo assessment of UVB-associated microvascular remodeling and its modulation by nitric oxide (NO) signaling remains limited.
OBJECTIVE: This study aimed to characterize UVB-induced cutaneous microvascular responses using multimodal in vivo imaging and graph-based vascular network analysis and to evaluate the effects of nitric oxide synthase (NOS) inhibition on these vascular responses.
METHODS: Seven-week-old male C57BL/6 mice were used for laser Doppler flowmetry (LDF), whereas seven-week-old female B6 nude mice were used for optical coherence tomography angiography (OCTA) and OCT structural imaging. In each modality-specific cohort, mice were allocated to control, UVB irradiation (200 mJ/cm2), UVB combined with topical Nω-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg), or L-NAME alone groups. Cutaneous perfusion was measured in dorsal skin by LDF at baseline and 24, 48, 72, and 96 h after intervention. OCTA and OCT imaging of the ear were performed at baseline and 48 h. OCTA images were analyzed using a graph-based framework to quantify node number, edge number, and total vessel length. Histological and immunohistochemical analyses for CD31 and inducible nitric oxide synthase (iNOS) were performed at 48 h.
RESULTS: UVB exposure significantly increased cutaneous perfusion at 48 h compared with the control group (p = 0.0164), whereas L-NAME attenuated this response (p = 0.0439 vs. UV). OCTA demonstrated greater visibility and extent of perfused superficial microvascular structures following UVB exposure, with apparent tissue thickening on structural OCT. Whole-image graph-based analysis showed modest positive changes in node number, edge number, and total vessel length in the UV group from baseline to 48 h, whereas the UV + L-NAME group showed decreases in all three network measures. These topology-derived changes were descriptive deterministic estimates rather than group-level inferential comparisons. Histological analyses demonstrated increased CD31-positive endothelial structures and iNOS immunoreactivity in UVB-exposed tissue.
CONCLUSIONS: Multimodal in vivo imaging combined with graph-based OCTA analysis enabled complementary assessment of UVB-associated changes in cutaneous perfusion and perfused microvascular network organization. The attenuation of UVB-associated hyperperfusion by L-NAME, together with the observed OCTA and histological findings, supports a contributory role of NOS-related signaling in UVB-associated cutaneous vascular dysregulation. Graph-based OCTA analysis may provide a useful approach for characterizing microvascular network alterations during cutaneous inflammatory responses.
OBJECTIVE: This study aimed to characterize UVB-induced cutaneous microvascular responses using multimodal in vivo imaging and graph-based vascular network analysis and to evaluate the effects of nitric oxide synthase (NOS) inhibition on these vascular responses.
METHODS: Seven-week-old male C57BL/6 mice were used for laser Doppler flowmetry (LDF), whereas seven-week-old female B6 nude mice were used for optical coherence tomography angiography (OCTA) and OCT structural imaging. In each modality-specific cohort, mice were allocated to control, UVB irradiation (200 mJ/cm2), UVB combined with topical Nω-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg), or L-NAME alone groups. Cutaneous perfusion was measured in dorsal skin by LDF at baseline and 24, 48, 72, and 96 h after intervention. OCTA and OCT imaging of the ear were performed at baseline and 48 h. OCTA images were analyzed using a graph-based framework to quantify node number, edge number, and total vessel length. Histological and immunohistochemical analyses for CD31 and inducible nitric oxide synthase (iNOS) were performed at 48 h.
RESULTS: UVB exposure significantly increased cutaneous perfusion at 48 h compared with the control group (p = 0.0164), whereas L-NAME attenuated this response (p = 0.0439 vs. UV). OCTA demonstrated greater visibility and extent of perfused superficial microvascular structures following UVB exposure, with apparent tissue thickening on structural OCT. Whole-image graph-based analysis showed modest positive changes in node number, edge number, and total vessel length in the UV group from baseline to 48 h, whereas the UV + L-NAME group showed decreases in all three network measures. These topology-derived changes were descriptive deterministic estimates rather than group-level inferential comparisons. Histological analyses demonstrated increased CD31-positive endothelial structures and iNOS immunoreactivity in UVB-exposed tissue.
CONCLUSIONS: Multimodal in vivo imaging combined with graph-based OCTA analysis enabled complementary assessment of UVB-associated changes in cutaneous perfusion and perfused microvascular network organization. The attenuation of UVB-associated hyperperfusion by L-NAME, together with the observed OCTA and histological findings, supports a contributory role of NOS-related signaling in UVB-associated cutaneous vascular dysregulation. Graph-based OCTA analysis may provide a useful approach for characterizing microvascular network alterations during cutaneous inflammatory responses.