Reciprocal interaction between vascular niche and sweat gland promotes sweat gland regeneration

The incorporation of vasculature is known to be effective in tissue or organ functional regeneration.However,a vague understanding of the interaction between epidermal appendages and their vascular niches is a foremost obstacle to obtaining sweat gland(SG)-specific vasculature units.Here,we map their precise anatomical con-nections and report that the interplay between SG cells(SGCs)and the surrounding vascular niche is key for glandular development and homeostasis maintenance.To replicate this interplay in vitro,we used three-dimensional(3D)bioprinting to generate reproducible SGC spheroids from differentiated adipose-derived mesenchymal stem cells(ADSCs).With dermal microvascular endothelial cells(DMECs),sacrificial templates made from poly(ε-caprolactone)(PCL)were fabricated to pattern the vascular niche.This interplay model promoted physiologically relevant vascularized glandular morphogenesis in vitro and in vivo.We identified a reciprocal regulatory mechanism for promoting SGs regeneration via contact-independent cell communication and direct cell-cell interactions between SGs and the vasculature.We envision the successful use of our approach for vascularized organ regeneration in the near future.

The human retinal stem niches could overlap a vascular anatomical pattern

Stem cells are undifferentiated cells which have the unique potential to self-renew and to supply, via intermediate stages of transit amplifying cells （TACs）, differentiated cells. With- in the stem cell niches not only heterologous cells, but also differentiated progeny of stem cells provide regulation to the stem cells parents. Stem cells can differentiate in various cell types during tissue maintenance or repair.

Abnormal bone marrow microenvironment: the “harbor” of acute lymphoblastic leukemia cells

Bone marrow(BM)microenvironment regulates and supports the production of blood cells which are necessary to maintain homeostasis.In analogy to normal hematopoiesis,leukemogenesis is originated from leukemic stem cells(LSCs)which gives rise to more differentiated malignant cells.Leukemia cells occupy BM niches and reconstruct them to support leukemogenesis.The abnormal BM niches are the main sanctuary of LSCs where they can evade chemotherapy-induced death and acquire drug resistance.In this review,we focus on the protective effects of BM niche cells on acute lymphoblastic leukemia cells.

Angiogenesis in acute myeloid leukemia

Angiogenesis is a word that refers to new blood vessel formation,and this process is of fundamental importance for physiological development and tissue homeostasis,as well as the genesis of several diseases,including tumors.Thus,studies carried out in the last years have shown that angiogenesis is essential for the growth of many solid tumors.Angiogenesis is also important for the growth of many hematological malignancies,including acute myeloid leukemia(AML).Endothelial cells are essential constituents of the bone marrow vascular niches,structures essential for the survival and maintenance of normal hematopoietic stem/progenitor cells.Bone marrow endothelial cells play an essential role in leukemia development and there is growing evidence that a targeting of both leukemic and endothelial cells of the leukemic vascular niche may improve the efficacy of antileukemic therapies.Bone marrow angiogenesis is frequently increased in AML,is morphologically evidenced as increased microvascular density,and is typically associated with some AML subtypes.The molecular mechanisms underlying the increased angiogenesis in some AML subtypes have been defined.In conclusion,a better understanding of angiogenesis as well as the fundamental interactions between bone marrow endothelial cells and leukemic stem cells may contribute to improve antileukemia treatments.