Tattoo aftercare management with a dermo‐cosmetic product: Improvement in discomfort sensation and skin repair quality

BACKGROUND: A moisturizer application during the healing process after a tattoo session is a common practice to help wound healing and to reduce discomfort sensations. This practice was recently recommended by the standard European guidelines on tattoos, with the use of an adapted ointment to keep the site moist. AIMS: To assess the efficacy and the tolerability of a specific dermo‐cosmetic product (Cicabio Pommade, Laboratoire Bioderma, NAOS, France) in tattoo aftercare. PATIENTS/METHODS: Thirty subjects included in this survey applied the product immediately after the tattoo session for 14 days. The objective symptoms (redness, edema, skin repair quality) were assessed by the tattooist and the subjects. The subjective symptoms, discomfort sensations (pain, itching, burning sensations, tingling), soothing, moisturizing, and undesirable effects were assessed by the tattooed individuals. RESULTS: After 14 days of application, redness was absent for 100% and 96% of subjects according to the tattoo artist and the subjects, respectively, and edema had completely disappeared for both assessors. Most of the subjects rated the skin quality repair and the aesthetic outcomes as very good to excellent. Soothing and moisturizing effects were observed as early as the first day. The effects were maintained over 14 days. Discomfort sensations were judged absent to slight in 96%–100% of cases after 7 days. They were assessed as absent to slight in all cases for pain, itching, and tingling, and in 96% for burning sensations after 14 days. The product was very well tolerated by 87% of the subjects. CONCLUSIONS: Our survey demonstrates that this dermo‐cosmetic product is suitable for tattooed skin aftercare as it reduced skin discomfort as soon as the first day and led to a good skin quality repair while being well tolerated

ALK1 controls hepatic vessel formation, angiodiversity, and angiocrine functions in hereditary hemorrhagic telangiectasia of the liver

Background and Aims In hereditary hemorrhagic telangiectasia (HHT), severe liver vascular malformations are associated with mutations in the Activin A Receptor-Like Type 1 (ACVRL1) gene encoding ALK1, the receptor for bone morphogenetic protein (BMP) 9/BMP10, which regulates blood vessel development. Here, we established an HHT mouse model with exclusive liver involvement and adequate life expectancy to investigate ALK1 signaling in liver vessel formation and metabolic function. Approach and Results Liver sinusoidal endothelial cell (LSEC)-selective Cre deleter line, Stab2-iCreF3, was crossed with Acvrl1-floxed mice to generate LSEC-specific Acvrl1-deficient mice (Alk1(HEC-KO)). Alk1(HEC-KO) mice revealed hepatic vascular malformations and increased posthepatic flow, causing right ventricular volume overload. Transcriptomic analyses demonstrated induction of proangiogenic/tip cell gene sets and arterialization of hepatic vessels at the expense of LSEC and central venous identities. Loss of LSEC angiokines Wnt2, Wnt9b, and R-spondin-3 (Rspo3) led to disruption of metabolic liver zonation in Alk1(HEC-KO) mice and in liver specimens of patients with HHT. Furthermore, prion-like protein doppel (Prnd) and placental growth factor (Pgf) were upregulated in Alk1(HEC-KO) hepatic endothelial cells, representing candidates driving the organ-specific pathogenesis of HHT. In LSEC in vitro, stimulation or inhibition of ALK1 signaling counter-regulated Inhibitors of DNA binding (ID)1-3, known Alk1 transcriptional targets. Stimulation of ALK1 signaling and inhibition of ID1-3 function confirmed regulation of Wnt2 and Rspo3 by the BMP9/ALK1/ID axis. Conclusions Hepatic endothelial ALK1 signaling protects from development of vascular malformations preserving organ-specific endothelial differentiation and angiocrine signaling. The long-term surviving Alk1(HEC-KO) HHT model offers opportunities to develop targeted therapies for this severe disease.Cancer Signaling networks and Molecular Therapeutic

ALK1 controls hepatic vessel formation, angiodiversity, and angiocrine functions in hereditary hemorrhagic telangiectasia of the liver

Background and Aims In hereditary hemorrhagic telangiectasia (HHT), severe liver vascular malformations are associated with mutations in the Activin A Receptor-Like Type 1 (ACVRL1) gene encoding ALK1, the receptor for bone morphogenetic protein (BMP) 9/BMP10, which regulates blood vessel development. Here, we established an HHT mouse model with exclusive liver involvement and adequate life expectancy to investigate ALK1 signaling in liver vessel formation and metabolic function. Approach and Results Liver sinusoidal endothelial cell (LSEC)-selective Cre deleter line, Stab2-iCreF3, was crossed with Acvrl1-floxed mice to generate LSEC-specific Acvrl1-deficient mice (Alk1(HEC-KO)). Alk1(HEC-KO) mice revealed hepatic vascular malformations and increased posthepatic flow, causing right ventricular volume overload. Transcriptomic analyses demonstrated induction of proangiogenic/tip cell gene sets and arterialization of hepatic vessels at the expense of LSEC and central venous identities. Loss of LSEC angiokines Wnt2, Wnt9b, and R-spondin-3 (Rspo3) led to disruption of metabolic liver zonation in Alk1(HEC-KO) mice and in liver specimens of patients with HHT. Furthermore, prion-like protein doppel (Prnd) and placental growth factor (Pgf) were upregulated in Alk1(HEC-KO) hepatic endothelial cells, representing candidates driving the organ-specific pathogenesis of HHT. In LSEC in vitro, stimulation or inhibition of ALK1 signaling counter-regulated Inhibitors of DNA binding (ID)1-3, known Alk1 transcriptional targets. Stimulation of ALK1 signaling and inhibition of ID1-3 function confirmed regulation of Wnt2 and Rspo3 by the BMP9/ALK1/ID axis. Conclusions Hepatic endothelial ALK1 signaling protects from development of vascular malformations preserving organ-specific endothelial differentiation and angiocrine signaling. The long-term surviving Alk1(HEC-KO) HHT model offers opportunities to develop targeted therapies for this severe disease