Ricardo Gutiérrez

Universidad de La Laguna

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Lucio Díaz‐Flores

Universidad de La Laguna

Juan Francisco Madrid

Universidad de Murcia

Miriam González‐Gómez

Universidad de La Laguna

José Luís Carrasco

Universidad de La Laguna

F. Valladares

Instituto de Salud Carlos III

HÁ

Hugo Álvarez‐Argüelles

Universidad de La Laguna

Francisco José Sáez

University of the Basque Country

H Varela

University of Pittsburgh

Pablo Martín‐Vasallo

Universidad de La Laguna

Maria Pino García

Hospiten Group

Cooperative Institutions

Universidad de La Laguna

Hospital Universitario de Canarias

Hospital San Agustin

Universidad Autónoma de Madrid

Marqués de Valdecilla University Hospital

Hospital Universitario Fundación Jiménez Díaz

Hospiten Group

Hospital Universitario de La Princesa

The University of Texas MD Anderson Cancer Center

Universidad de Cantabria

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Review Adult stem and transit-amplifying cell location

Lucio Díaz‐Flores Ricardo Gutiérrez H Varela F. Valladares Hugo Álvarez‐Argüelles

Summary. Adult stem cells (ASC) -able to self renew and to intervene in maintaining the structural and functional integrity of their original tissue- can express greater plasticity than traditionally attributed to them, adopting functional phenotypes and expression profiles of cells from other tissues. Therefore, they could be useful to regenerative medicine and tissue engineering. Transit-amplifying cells (TAC) are committed progenitors among the ASC and their terminally differentiated daughter cells. The ASC reside in a specialized physical location named niche, which constitutes a three-dimensional microenviroment where ASC and TAC are protected and controlled in their selfrenewing capacity and differentiation. The niche can be located near or far from the recruitment point, requiring a short or long-distance cellular migration, respectively. This paper briefly reviews the current status of research about ASC plasticity, transdifferentiation, fusion and functional adaptation mechanisms. Subsequently, ASC and TAC occurrence, characteristics and location have been considered in the skin, cornea, respiratory tract, teeth, gastrointestinal tract, liver, pancreas, salivary glands, kidney, breast, prostate, endometrium, mesenchyma, bone marrow, skeletal and cardiac muscle, nervous system and pituitary gland. Moreover, the role of cancer ASC has also been revised.

Regenerative Medicine

Transdifferentiation

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CD34‐positive fibroblasts in Reinke's edema

The Laryngoscope (2013)

Lucio Díaz‐Flores Ricardo Gutiérrez Maria del Pino García Hugo Álvarez‐Argüelles Lucio Díaz‐Flores

To elucidate whether and to what extent CD34+ fibroblasts (so-called CD34+ fibrocytes, CD34+ dendritic cells, and CD34+ stromal cells) occur in normal human vocal folds and in Reinke's edema.Histological study.Conventional, immunohistochemical, and ultrastructural procedures were performed in histological blocks of 18 selected cases of Reinke's edema (with typical findings including acellular edematous spaces in the subepithelial connective tissue of vocal folds, and disarrangement of elastic, collagen, and reticular fibers). For control purposes, four normal vocal folds were analyzed.In normal vocal folds, most stromal cells were spindle-shaped CD34+ fibroblasts. In Reinke's edema, increased density and changes in the morphology and size of this subpopulation of fibroblasts were demonstrated in the connective tissue surrounding the edematous spaces, particularly in their borders, where together with some macrophages they formed boundaries, mimicking the walls of distended lymphatic vessels when conventional stains were used. These activated CD34+ fibroblasts acquired a dendritic morphology (with long, moniliform, often bifurcated, overlapping multipolar processes), and their cytoplasmic organelles were increased in number. In addition to CD34, they expressed vimentin, CD10 and CD99, but no α-smooth muscle actin (α-SMA), CD31, CD117, CD68, h-caldesmon, desmin, or S-100 protein.CD34+ fibroblasts are a major cell component in the stroma of vocal folds in Reinke's edema, and their activation, with increased density and morphologic changes around the edematous spaces, occurs without immunophenotypic transformation toward myofibroblasts (no expression of α-SMA). The mechanisms by which these cells act in Reinke's edema require further study.

Fibrocyte

Myofibroblast

Vocal folds

Reticular connective tissue

Desmin

10.1002/lary.24407

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Citations (14)

Localized amyloidosis of the epididymis: a previously unreported phenomenon

Diagnostic Pathology (2017)

Lucio Díaz‐Flores Ricardo Gutiérrez Ma. del Pino García Manuel J. Gayoso José Luís Carrasco

Localized amyloidosis has not been documented in the epididymis; we report this phenomenon for the first time. The first aim of this work is to report three cases of localized epididymal amyloidosis. Two cases were clinically detected as epididymal nodules, and a third after reviewing 120 epididymides obtained with neighbouring pathological processes. Amyloid deposits showed Congo red positivity, with yellow-green birefringence, and immunohistochemical expression for light chains kappa and lambda, transthyretin, amyloid P and cytokeratin AE1 AE3. No immunoreactivity for amyloid A was seen. Amyloid deposit location was intraluminal, with partial or total loss of the epididymal epithelium and subsequent passage to the interstitium, forming large masses. No amyloid deposits were observed around blood vessels. A secondary objective was to explore in normal epididymis the amyloid tested in epididymal amyloidosis. In normal epididymides, expression of amyloid P and transthyretin was detected in the apical surface of epithelial cells. Amyloid P also showed strong expression in spermatozoa. We contribute the existence of localized epididymal amyloidosis, which presents a distinctive, initial intratubular location, where there is a unique proteome and where functional amyloids act during sperm maturation.

Amyloid (mycology)

Amyloid disease

10.1186/s13000-017-0646-z

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Pólipo fibroepitelial de uretra en un adulto

Actas Urológicas Españolas (2003)

José Manuel Lanzas Prieto C.L. Menéndez Fernández F.J. Pérez García Ricardo Gutiérrez J. González tuero

10.1016/s0210-4806(03)72991-x

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Adult stem and transit-amplifying cells in repair through granulation tissue: Role of the pericytic vasculature niche

Lucio Díaz‐Flores Ricardo Gutiérrez Juan Francisco Madrid Hugo Álvarez‐Argüelles F. Valladares

In this section, granulation tissue is considered as a structural proliferative unit in which the transit-amplifying cells (TACs) are well known while the adult stem cells (ASCs) and the ASC niche are difficult to identify. We describe the morphofunctional sequence of the TACs (TA-endothelial cells-TAECs, TA-pericytes, TA-fibroblasts/myofibroblasts, TA-monocytes/macrophages) in the pre-existing pericytic vasculature (contemplated as a crossroads) and subsequently in the granulation tissue (in the sprouting, newly-formed, stabilized and involutive vessels, and in the intervascular spaces). We then consider the most broadly held origin (progenitor cells/ASCs) of the TAC endothelial cells (preexisting ECs and bone marrow endothelial progenitor cells-EPCs) and of the TA-pericytes and TA-fibroblasts/myofibroblasts (pericytes/vascular smooth muscle cells, fibroblasts, bone marrow mesenchymal cells). We conclude the origin of these cells with a unitary hypothesis: Pericytic microvasculature as an ASC niche and transit point of precursor cells. Finally, we take into account the pathological implications (e.g. in abnormal repair, atherosclerosis, and tumors) and therapeutic promises. © 2011 by Nova Science Publishers, Inc. All rights reserved.

Pericyte

Myofibroblast

Granulation tissue

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Pericytes. Morphofunction, interactions and pathology in a quiescent and activated mesenchymal cell niche.

PubMed (2009)

Lucio Díaz‐Flores Ricardo Gutiérrez Juan Francisco Madrid H Varela F. Valladares

We review the morphofunctional characteristics of pericytes and report our observations. After a brief historical background, we consider the following aspects of pericytes: A) Origin in embryonic vasculogenesis (mesenchymal stem cells, neurocrest and other possible sources) and in embryonic and postnatal life angiogenesis (pre-existing pericytes, fibroblast/ myofibroblasts and circulating progenitor cells). B) Location in pericytic microvasculature and in the other blood vessels (including transitional cell forms and absence in lymphatic vessels), incidence (differences depending on species, topographical location, and type and stage of vessels) and distribution (specific polarities) in blood vessels. C) Morphology (cell body, and longitudinal and circumferential cytoplasmic processes), structure (nucleus, cytoplasmic organelles and distribution of microtubules, intermediate filaments and microfilaments) and surface (caveolae system). D) Basement membrane disposition, formation, components and functions. E) Contacts with endothelial cells (ECs) (peg and socket arrangements, adherent junctions and gap junctions) and with basal membrane (adhesion plaques). F) Molecular expression (pericyte marker identification). G) Functions, such as vessel stabilization, regulation of vascular tone and maintenance of local and tissue homeostasis (contractile capacity and vessel permeability regulation), matrix protein synthesis, macrophage-like properties, immunological defense, intervention in coagulation, participation in mechanisms that regulate the quiescent and angiogenic stages of blood vessels (including the behaviour of pericytes during sprouting angiogenesis and intussuceptive vascular growth, as well as pericyte interactions with endothelium and other cells, and with extracellular matrix) and plasticity, as progenitor cells with great mesenchymal potential, originating other pericytes, fibroblast/myofibroblasts, preadipocytes, chondroblasts, osteoblasts, odontoblasts, vascular smooth muscle and myointimal cells. This mesenchymal capacity is seen in a broad section on the perivascular mesenchymal cell niche hypothesis and in the concept of pericyte and EC "marriage and divorce". H) Peculiar pericyte types, such as hepatic stellate cells (Ito cells), bone marrow reticular cells and mesangial cells. I) Involvement in pathological processes, such as repair through granulation tissue, pericyte-derived tumors, tumor angiogenesis and tumoral cell metastasis, diabetic microangiopathy, fibrosis, atherosclerosis and calcific vasculopathy, lymphedema distichiasis, chronic venous insufficiency, pulmonary hypertension, Alzheimer disease and multiple sclerosis. J) Clinical and therapeutic implications (de-stabilization of vessels or formation of a stable vasculature).

Pericyte

Vasculogenesis

Sprouting angiogenesis

10.14670/hh-24.909

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Citations (535)

Morphofunctional basis of the different types of angiogenesis and formation of postnatal angiogenesis-related secondary structures.

PubMed (2017)

Lucio Díaz‐Flores Ricardo Gutiérrez M P García-Suárez Francisco José Sáez E Gutiérrez

We review the morpho-functional basis of the different types of angiogenesis and report our observations, including the formation of angiogenesis-related secondary structures. First of all, we consider the following issues: a) conceptual differences between angiogenesis and vasculogenesis, b) incidence of angiogenesis in pre- and postnatal life, c) regions of vascular tree with angiogenic capacity, d) cells (endothelial cells, pericytes, CD34+ adventitial stromal cells of the microvasculature and inflammatory cells) and extracellular matrix components involved in angiogenesis, e) events associated with angiogenesis, f) different types of angiogenesis, including sprouting and intussusceptive angiogenesis, and other angiogenic or vascularization forms arising from endothelial precursor cells (postnatal vasculogenesis), vasculogenesis mimicry, vessel co-option and piecemeal angiogenesis. Subsequently, we consider the specific morpho-functional characteristics of each type of angiogenesis. In sprouting angiogenesis, we grouped the events in three phases: a) activation phase, which includes vasodilation and increased permeability, EC, pericyte and CD34+ adventitial stromal cell activation, and recruitment and activation of inflammatory cells, b) sprouting phase, encompassing EC migration (concept and characteristics of endothelial tip cells, tip cell selection, lateral inhibition, localized filopodia formation, basal lamina degradation and extracellular changes facilitating EC migration), EC proliferation (concept of endothelial stalk cells), pericyte mobilization, proliferation, recruitment and changes in CD34+ adventitial stromal cells and inflammatory cells, tubulogenesis, formation of a new basal lamina, and vascular anastomosis with capillary loop formation, and c) vascular remodelling and stabilization phase (concept of phalanx cells). Subsequently, the concept, incidence, events and mechanisms are considered in the other forms of angiogenesis. Finally, we contribute the formation of postnatal angiogenesis-related secondary structures: a) intravascular structures through piecemeal angiogenesis, including intravascular papillae in vessel tumours and pseudotumours (intravascular papillary endothelial hyperplasia, vascular transformation of the sinus in lymph nodes, papillary intralymphatic angioendothelioma or Dabska tumour, retiform hemangioendothelioma, hemangiosarcoma and lymphangiosarcoma), vascular septa in hemorrhoidal veins and intravascular projections in some tumours; b) arterial intimal thickening; c) intravascular tumours and pseudotumours (e.g. intravenous pyogenic granulomas and intravascular myopericytoma); d) vascular glomeruloid proliferations; and e) pseudopalisading necrosis in glioblastoma multiform.

Vasculogenesis

Sprouting angiogenesis

Pericyte

10.14670/hh-11-923

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Citations (34)

Comparison of the Behavior of Perivascular Cells (Pericytes and CD34+ Stromal Cell/Telocytes) in Sprouting and Intussusceptive Angiogenesis

International Journal of Molecular Sciences (2022)

Lucio Díaz‐Flores Ricardo Gutiérrez Maria Pino García Miriam González‐Gómez Lucio Díaz‐Flores

Perivascular cells in the pericytic microvasculature, pericytes and CD34+ stromal cells/telocytes (CD34+SCs/TCs), have an important role in angiogenesis. We compare the behavior of these cells depending on whether the growth of endothelial cells (ECs) from the pre-existing microvasculature is toward the interstitium with vascular bud and neovessel formation (sprouting angiogenesis) or toward the vascular lumen with intravascular pillar development and vessel division (intussusceptive angiogenesis). Detachment from the vascular wall, mobilization, proliferation, recruitment, and differentiation of pericytes and CD34+SCs/TCs, as well as associated changes in vessel permeability and functionality, and modifications of the extracellular matrix are more intense, longer lasting over time, and with a greater energy cost in sprouting angiogenesis than in intussusceptive angiogenesis, in which some of the aforementioned events do not occur or are compensated for by others (e.g., sparse EC and pericyte proliferation by cell elongation and thinning). The governing mechanisms involve cell–cell contacts (e.g., peg-and-socket junctions between pericytes and ECs), multiple autocrine and paracrine signaling molecules and pathways (e.g., vascular endothelial growth factor, platelet-derived growth factor, angiopoietins, transforming growth factor B, ephrins, semaphorins, and metalloproteinases), and other factors (e.g., hypoxia, vascular patency, and blood flow). Pericytes participate in vessel development, stabilization, maturation and regression in sprouting angiogenesis, and in interstitial tissue structure formation of the pillar core in intussusceptive angiogenesis. In sprouting angiogenesis, proliferating perivascular CD34+SCs/TCs are an important source of stromal cells during repair through granulation tissue formation and of cancer-associated fibroblasts (CAFs) in tumors. Conversely, CD34+SCs/TCs have less participation as precursor cells in intussusceptive angiogenesis. The dysfunction of these mechanisms is involved in several diseases, including neoplasms, with therapeutic implications.

Sprouting angiogenesis

Pericyte

10.3390/ijms23169010

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Citations (15)

Dorsal root ganglion inflammation by oxaliplatin toxicity: DPEP1 as possible target for peripheral neuropathy prevention

BMC Neuroscience (2024)

Karen Álvarez-Tosco Rebeca González-Fernández María Ángeles González-Nicolás Rita Martín-Ramírez Manuel Morales

Dorsal root ganglion

10.1186/s12868-024-00891-y

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Las células de Leydig ováricas

Majorensis: Revista Electrónica de Ciencia y Tecnología (2017)

Cristina Alemán Sánchez Íñigo Hernández Gabriel Marrero Fraga Carmen Martín Corriente Hugo Álvarez-Argüelles Cabrera

espanolHemos efectuado un estudio morfologico, con microscopia optica convencional, de preparaciones histologicas de tejido ovarico humano incluido en bloques de parafina. Son muestras obtenidas y utilizadas para fines clinicos, habiendose mantenido un completo anonimato de las pacientes. Hemos concentrado el estudio en las celulas de Leydig del ovario, en su patologia no tumoral y en su posible relacion con otras patologias ginecologicas. Los hallazgos obtenidos nos permiten establecer una relacion entre la hiperplasia de las celulas de Leydig ovaricas con la hiperplasia del estroma cortical ovarico y con el carcinoma endometrioide de endometrio (Tipo I). EnglishWe performed a morphological study, using conventional optical microscopy and histological preparations of human ovarian tissue included in paraffin blocks. These are samples obtained and used for clinical purposes, with complete patient anonymity. We have focused the study on the Leydig cells of the ovary, its non-tumor pathology and its possible relation with other gynecological pathologies. The findings obtained allow us to establish a relationship between ovarian Leydig cell hyperplasia with ovarian cortical stromal hyperplasia and endometrioid endometrial carcinoma (Type I).

Endometrial hyperplasia

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