Telocyte Behaviour During Inflammation, Repair and Tumour Stroma Formation.

In this chapter, we outline the role of human CD34+ stromal cells/telocytes (CD34+ SC/TCs) as progenitor cells during repair. The in vivo activation phenomena of CD34+ SC/TCs in this process include increased size; separation from the neighbouring structures (mainly of the vascular walls); association with inflammatory cells, predominantly macrophages; development of the organelles of synthesis (rough endoplasmic reticulum and Golgi apparatus); cell proliferation with presence of mitosis and high proliferative index (transit-amplifying cells); and fibroblastic and myofibroblastic differentiation. A procedure to study these tissue-resident cells, comparison of their behaviour in vivo and in vitro and different behaviour depending on location, time, type of injury (including tumour stroma) and greater or lesser proximity to the injury are also considered.

Participation of angiogenesis from rat femoral veins in the neovascularization of adjacent occluded arteries.

The neovascularization of the arterial wall in human and experimental pathology has been demonstrated. The occlusion of the of the rat femoral artery is a suitable model for the study of these angiogenesis processes. Newly formed capillaries growing into the arterial wall have been described in this model. The origin of these ingrowing capillaries has been attribute to the preformed surrounding venules and capillaries. The contribution of the adjacent femoral vein with a supplementary population of vascular sprouts could also be possible. To test this hypothesis in half of the occluded arteries, the adventitia was removed from the side facing the femoral vein. Between 1 and 3 days after surgery several alterations were found both in the endothelial cells and the smooth muscle cells of the tunica media. Between 3 and 6 days, solid or canalized endothelial sprouts were observed arising from the femoral vein. By days 4 and 6, newly formed capillaries grew into the adventitia and tunica media of the femoral artery. Some of them, penetrated the internal elastic lamina. This microvascular penetration from the femoral vein was more prominent in the area of the ostium of the collateral and when the adventitia was removed. Some ingrowing capillaries were in continuity with the endothelial cells of the arterial neointima. At days 7 and 8, regressing capillaries were observed in the neomicrovasculature network between artery and vein, with a selective loss of the smaller vessels. From day 9 onwards, fewer and larger vascular channels were present between the femoral vein and the femoral artery. An arterial neolumen contained what appeared to be circulating "fresh" blood. Quantitatively, the venous neocapillary density increased from days 4 to 6 and then declined significantly by day 8. The arterial neocapillary density increased form days 4 to 8 and declined significantly by day 12. Moreover, both densities were significantly greater when the arterial adventitia was removed. The perfusion with barium solution showed the presence of the contrast material in the newly formed vessels, the lumen of the femoral vein, and the neolumen of the occluded arterial segment. The present findings indicate that putative angiogenic molecules released form the occluded arterial segment may reach the adjacent wall of the vein inducing neovascularization from it. The vein vascular sprouts are connected to the ingrowing capillaries in the occluded arterial wall and to the neocapillaries form the preexisting pericytic microvasculature. When the arterial adventitia were removed up to 2 times greater vein neocapillary's density was observed suggesting an easily access of the putative angiogenic factors to the vein.