Inventors show that both iKO and Eng+ / - experienced increased bleeding compared to WT mice (longer bleeding times, more rebleeding events, greater
hemoglobin loss, p<0.05). Treatment with pEng effectively reduced bleeding in all genotypes (p<0.05), reverting to the control WT condition. Furthermore, pEng induced strong
platelet aggregation in both murine and human platelets compared to controls (p<0.01), demonstrating its
efficacy in promoting
hemostasis. No differences were found in term of co-culture,
wound healing and
sprouting considering controls and endoglin siRNA ECs, while a beneficial effect on ENG-free endothelial cells was found in capillary flow conditions, restoring the control condition. Accordingly, pEng appears to be a promising treatment for epistaxis in HHT, without deleterious effect on EC tested functions. The present invention relates to
a peptide derived from endoglin (pEng) comprising at least the
amino acid sequence X1-X2-X3-X4-X5-X6-X7-X8-X9-X10 (SEQ ID NO: 1) wherein X1 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X2 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X3 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X4 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X5 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X6 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X7 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X8 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X9 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), X10 is Phe (F), Tyr(Y), His(H), Thr(T), Ser(S), Leu(L), or Val (V), Wherein
peptide derived from endoglin (pEng) comprises at least one of each Phe(F), Leu(L), Tyr(Y), His(H), Thr(T), Ser(S), and Val(V).