scholarly journals The Telocytes in the Subepicardial Niche

2019 ◽  
Vol 9 (8) ◽  
pp. 1615 ◽  
Author(s):  
Cristian Bogdan Iancu ◽  
Mugurel Constantin Rusu ◽  
Laurenţiu Mogoantă ◽  
Sorin Hostiuc ◽  
Oana Daniela Toader
Keyword(s):  
Stromal Cells ◽  
Lymphatic Vessels ◽  
Growth Factor Receptor ◽  
Immunohistochemical Method ◽  
Lymphatic Endothelial Cells ◽  
Cell Type ◽  
Ki 67 ◽  
Epicardial Cells ◽  
Immunohistochemical Evidence ◽  
Unique Cell

A great interest has developed over the last several years in research on interstitial Cajal-like cells (ICLCs), later renamed to telocytes (TCs). Such studies are restricted by diverse limitations. We aimed to critically review (sub)epicardial ICLCs/TCs and to bring forward supplemental immunohistochemical evidence on (sub)epicardial stromal niche inhabitants. We tested the epicardial expressions of CD117/c-kit, CD34, Cytokeratin 7 (CK7), Ki67, Platelet-Derived Growth Factor Receptor (PDGFR)-α and D2-40 in adult human cardiac samples. The mesothelial epicardial cells expressed D2-40, CK7, CD117/c-kit and PDGFR-α. Subepicardial D2-40-positive lymphatic vessels and isolated D2-40-positive and CK7-positive subepicardial cells were also found. Immediate submesothelial spindle-shaped cells expressed Ki-67. Submesothelial stromal cells and endothelial tubes were PDGFR-α-positive and CD34-positive. The expression of CD34 was pan-stromal, so a particular stromal cell type could not be distinguished. The stromal expression of CD117/c-kit was also noted. It seems that epicardial TCs could not be regarded as belonging to a unique cell type until (pre)lymphatic endothelial cells are inadequately excluded. Markers such as CD117/c-kit or CD34 seem to be improper for identifying TCs as a distinctive cell type. Care should be taken when using the immunohistochemical method and histological interpretations, as they may not produce accurate results.

scholarly journals Structural and functional conservation of non-lumenized lymphatic endothelial cells in the mammalian leptomeninges

2019 ◽  
Vol 139 (2) ◽  
pp. 383-401 ◽  
Author(s):  
Shannon Shibata-Germanos ◽  
James R. Goodman ◽  
Alan Grieg ◽  
Chintan A. Trivedi ◽  
Bridget C. Benson ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Dura Mater ◽  
Lymphatic Vessels ◽  
Amyloid Β ◽  
Lymphatic Endothelial Cells ◽  
Cell Type ◽  
Functional Conservation ◽  
Spherical Inclusions ◽  
Lymphatic Markers ◽  
The Brain

Abstract The vertebrate CNS is surrounded by the meninges, a protective barrier comprised of the outer dura mater and the inner leptomeninges, which includes the arachnoid and pial layers. While the dura mater contains lymphatic vessels, no conventional lymphatics have been found within the brain or leptomeninges. However, non-lumenized cells called Brain/Mural Lymphatic Endothelial Cells or Fluorescent Granule Perithelial cells (muLECs/BLECs/FGPs) that share a developmental program and gene expression with peripheral lymphatic vessels have been described in the meninges of zebrafish. Here we identify a structurally and functionally similar cell type in the mammalian leptomeninges that we name Leptomeningeal Lymphatic Endothelial Cells (LLEC). As in zebrafish, LLECs express multiple lymphatic markers, containing very large, spherical inclusions, and develop independently from the meningeal macrophage lineage. Mouse LLECs also internalize macromolecules from the cerebrospinal fluid, including Amyloid-β, the toxic driver of Alzheimer’s disease progression. Finally, we identify morphologically similar cells co-expressing LLEC markers in human post-mortem leptomeninges. Given that LLECs share molecular, morphological, and functional characteristics with both lymphatics and macrophages, we propose they represent a novel, evolutionary conserved cell type with potential roles in homeostasis and immune organization of the meninges.

scholarly journals Inflammation induces lymphangiogenesis through up-regulation of VEGFR-3 mediated by NF-κB and Prox1

Blood ◽  
2010 ◽  
Vol 115 (2) ◽  
pp. 418-429 ◽  
Author(s):  
Michael J. Flister ◽  
Andrew Wilber ◽  
Kelly L. Hall ◽  
Caname Iwata ◽  
Kohei Miyazono ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Time Course ◽  
Molecular Mechanisms ◽  
Lymphatic Vessels ◽  
Growth Factor Receptor ◽  
Receptor Expression ◽  
Lymphatic Endothelial Cells ◽  
Inflammatory Stimuli ◽  
And Migration

Abstract The concept of inflammation-induced lymphangiogenesis (ie, formation of new lymphatic vessels) has long been recognized, but the molecular mechanisms remained largely unknown. The 2 primary mediators of lymphangiogenesis are vascular endothelial growth factor receptor-3 (VEGFR-3) and Prox1. The key factors that regulate inflammation-induced transcription are members of the nuclear factor-kappaB (NF-κB) family; however, the role of NF-κB in regulation of lymphatic-specific genes has not been defined. Here, we identified VEGFR-3 and Prox1 as downstream targets of the NF-κB pathway. In vivo time-course analysis of inflammation-induced lymphangiogenesis showed activation of NF-κB followed by sequential up-regulation of Prox1 and VEGFR-3 that preceded lymphangiogenesis by 4 and 2 days, respectively. Activation of NF-κB by inflammatory stimuli also elevated Prox1 and VEGFR-3 expression in cultured lymphatic endothelial cells, resulting in increased proliferation and migration. We also show that Prox1 synergizes with the p50 of NF-κB to control VEGFR-3 expression. Collectively, our findings suggest that induction of the NF-κB pathway by inflammatory stimuli activates Prox1, and both NF-κB and Prox1 activate the VEGFR-3 promoter leading to increased receptor expression in lymphatic endothelial cells. This, in turn, enhances the responsiveness of preexisting lymphatic endothelium to VEGFR-3 binding factors, VEGF-C and VEGF-D, ultimately resulting in robust lymphangiogenesis.

scholarly journals Circadian clocks guide dendritic cells into skin lymphatics

2021 ◽  
Author(s):  
Stephan J. Holtkamp ◽  
Louise M. Ince ◽  
Coline Barnoud ◽  
Madeleine T. Schmitt ◽  
Flore Sinturel ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Immune Responses ◽  
Lymphatic Vessels ◽  
Migration Pattern ◽  
Circadian Clocks ◽  
Leukocyte Trafficking ◽  
Lymphatic Endothelial Cells ◽  
Cell Type ◽  
Adaptive Immune Responses ◽  
Adaptive Immune

AbstractMigration of leukocytes from the skin to lymph nodes (LNs) via afferent lymphatic vessels (LVs) is pivotal for adaptive immune responses1,2. Circadian rhythms have emerged as important regulators of leukocyte trafficking to LNs via the blood3,4. Here, we demonstrate that dendritic cells (DCs) have a circadian migration pattern into LVs, which peaks during the rest phase in mice. This migration pattern is determined by rhythmic gradients in the expression of the chemokine CCL21 and of adhesion molecules in both mice and humans. Chronopharmacological targeting of the involved factors abrogates circadian migration of DCs. We identify cell-intrinsic circadian oscillations in skin lymphatic endothelial cells (LECs) and DCs that cogovern these rhythms, as their genetic disruption in either cell type ablates circadian trafficking. These observations indicate that circadian clocks control the infiltration of DCs into skin lymphatics, a process that is essential for many adaptive immune responses and relevant for vaccination and immunotherapies.

Placental Transmogrification of the Lung Is a Histologic Pattern Frequently Associated With Pulmonary Fibrochondromatous Hamartoma

2002 ◽  
Vol 126 (5) ◽  
pp. 562-566 ◽  
Author(s):  
Ruliang Xu ◽  
Melissa Murray ◽  
Jaishree Jagirdar ◽  
Yara Delgado ◽  
Jonathan Melamed
Keyword(s):  
Mast Cells ◽  
Stromal Cells ◽  
Polyclonal Antibodies ◽  
Growth Factor Receptor ◽  
Immunohistochemical Analysis ◽  
Lung Parenchyma ◽  
Ki 67 ◽  
Thyroid Transcription Factor 1 ◽  
Histologic Pattern ◽  
Rare Cells

Abstract Context.—Placental transmogrification of the lung is a term introduced to describe a peculiar histologic pattern characterized by formation of placental villuslike structures in the lung parenchyma. It has been reported to occur in association with bullous emphysema and lipomatosis. Objectives.—To study the relationship between placental transmogrification and pulmonary hamartomas. Design and Methods.—Reports of 38 cases of pulmonary hamartomas during 18 years (1982–1999) were reviewed. All histologic slides of these cases were examined for the presence of villuslike papillary projections and placenta-like structures. Hamartomas with prominent papillary projections or placenta-like structures were further investigated to assess the histogenesis and proliferation of epithelial and stromal cells. Immunohistochemical analysis was performed on paraffin-embedded tissue using monoclonal antibodies against Ki-67 and thyroid transcription factor 1 (TTF-1) and polyclonal antibodies against c-Kit antigen (a stem cell factor receptor/mast cell growth factor receptor) in conjunction with Leder stain for naphthol-ASD-chloroacetate esterase. Results.—Placental transmogrification was identified in 6 of 38 cases of pulmonary fibrochondromatous hamartomas. The histologic change consisted of an abundant myxoid or edematous fibroadipose stroma with a respiratory epithelial lining, resulting in papillary projections that resembled immature placental villi. Epithelium lining the papillary projections was positive for TTF-1 (70%–90%) and Ki-67 (3%–5%). In contrast, stromal cells were negative for TTF-1 with only rare cells immunoreactive for Ki-67. A number of stromal spindle cells and occasional cells in epithelium were c-Kit immunoreactive; however, concurrent Leder stain demonstrated that these c-Kit–positive cells were mast cells and not stem cells. Conclusions.—Placental transmogrification is frequently associated with pulmonary fibrochondromatous hamartomas and may be induced by or associated with a proliferation of lining epithelial components in the hamartomas. The significance of numerous mast cells within stroma of placental transmogrification is unclear and their possible role in inducing stromal proliferation needs to be further evaluated.

scholarly journals Osteogenic differentiation of human mesenchymal stromal cells and fibroblasts differs depending on tissue origin and replicative senescence

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vera Grotheer ◽  
Nadine Skrynecki ◽  
Lisa Oezel ◽  
Jan Grassmann ◽  
Joachim Windolf ◽  
...  
Keyword(s):  
Cell Culture ◽  
Osteogenic Differentiation ◽  
Stromal Cells ◽  
Replicative Senescence ◽  
Cell Type ◽  
Differentiation Potential ◽  
Culture Passage ◽  
Cell Type Specific ◽  
Cell Culture Passage ◽  
Tissue Origin

AbstractThe need for an autologous cell source for bone tissue engineering and medical applications has led researchers to explore multipotent mesenchymal stromal cells (MSC), which show stem cell plasticity, in various human tissues. However, MSC with different tissue origins vary in their biological properties and their capability for osteogenic differentiation. Furthermore, MSC-based therapies require large-scale ex vivo expansion, accompanied by cell type-specific replicative senescence, which affects osteogenic differentiation. To elucidate cell type-specific differences in the osteogenic differentiation potential and replicative senescence, we analysed the impact of BMP and TGF-β signaling in adipose-derived stromal cells (ASC), fibroblasts (FB), and dental pulp stromal cells (DSC). We used inhibitors of BMP and TGF-β signaling, such as SB431542, dorsomorphin and/or a supplemental addition of BMP-2. The expression of high-affinity binding receptors for BMP-2 and calcium deposition with alizarin red S were evaluated to assess osteogenic differentiation potential. Our study demonstrated that TGF-β signaling inhibits osteogenic differentiation of ASC, DSC and FB in the early cell culture passages. Moreover, DSC had the best osteogenic differentiation potential and an activation of BMP signaling with BMP-2 could further enhance this capacity. This phenomenon is likely due to an increased expression of activin receptor-like kinase-3 and -6. However, in DSC with replicative senescence (in cell culture passage 10), osteogenic differentiation sharply decreased, and the simultaneous use of BMP-2 and SB431542 did not result in further improvement of this process. In comparison, ASC retain a similar osteogenic differentiation potential regardless of whether they were in the early (cell culture passage 3) or later (cell culture passage 10) stages. Our study elucidated that ASC, DSC, and FB vary functionally in their osteogenic differentiation, depending on their tissue origin and replicative senescence. Therefore, our study provides important insights for cell-based therapies to optimize prospective bone tissue engineering strategies.

Analysis of the effect of DEK overexpression on the survival and proliferation of bone marrow stromal cells

2019 ◽  
Vol 44 (4) ◽  
pp. 510-516
Author(s):  
Türkan Çakar ◽  
Ayten Kandilci
Keyword(s):  
Cell Lines ◽  
Stromal Cells ◽  
Cell Sorting ◽  
Bone Marrow Stromal Cells ◽  
Nuclear Protein ◽  
Cell Type ◽  
Facs Analysis ◽  
Periodic Growth ◽  
Stromal Cell Line ◽  
Rpmi 8226

Abstract Objective DEK is ubiquitously expressed and encodes a nuclear protein, which is also released from some cells. Overexpression of DEK suppresses proliferation of some blood cell progenitors whereas it increases proliferation of epithelial tumors. We showed that DEK is overexpressed in BM cells of 12% of multiple myeloma (MM) patients. Here, we aimed to test if DEK overexpression effects the proliferation and viability of BM stromal cells or MM cells co-cultured with DEK-overexpressing stromal cells, mimicking the BM microenvironment. Methods DEK is stably overexpressed in the BM stromal cell line HS27A. Periodic growth curve and fluorescent activated cell sorting (FACS) analysis was performed to determine the effect of DEK overexpression on HS27A cells and MM cell lines (RPMI-8226 and U266) that are co-cultured with these HS27A cells. Results We showed that, on the contrary to blood progenitors or ephitelial cells, DEK overexpression doesn’t alter the viability or proliferation of the HS27A cells, or the MM cell lines which are co-cultured with DEK-overexpressing HS27A cells. Conclusions Our results suggest that effect of DEK overexpression on the proliferation is cell type and context dependent and increased DEK expression is tolerable by the stromal cells and the co-cultured MM cell lines without effecting proliferation and viability.

ORAL CANCER BIOCHEMICAL RESEARCH: CURRENT STATUS AND EMERGING FRONTIERS

2021 ◽  
Vol 1 (1) ◽  
pp. 10-16
Author(s):  
Radu Radulescu ◽  
Alexandra Totan ◽  
Daniela Miricescu ◽  
Maria Greabu
Keyword(s):  
Oral Cancer ◽  
Treatment Options ◽  
Growth Factor Receptor ◽  
B Cell Lymphoma ◽  
Current Status ◽  
Inflammatory Factors ◽  
Ki 67 ◽  
Proliferation Markers ◽  
Genomic Markers ◽  
Biochemical Research

Cancer represents one of the leading causes or mortality worldwide, oral cancer accounting for almost 9% of deaths, early diagnosis playing a crucial role. Salivary biomarkers analysis is proving to be an alternative diagnosis method. Oral cancer biomarkers can be compounds that play role in every aspect of malignancy from triggering factors to markers of progression, inflammation or invasiveness. There are numerous genomic markers, ranging from well known ones such as p16, p21, p27 and p53 genes, cyclin D1, EGFR gene (epidermal growth factor receptor), C-kit gene (KIT proto-oncogene, receptor tyrosine kinase), bcl-6(B-cell lymphoma 6 protein gene) to least studied ones such as OXSR1(oxidative stress-responsive kinase-1gene). Proteomic markers range from inflammatory factors such as interleukins IL-8 and Il-6, transcription factors such as FOXO3 (forkhead box O3) protein and S100B protein, matrix metalloproteinases (MMP) involved in extracellular matrix degradation and their inhibitors (TIMP - tissue inhibitor of metalloproteinases), specific proliferation markers such as Ki-67 protein and many more. Developing saliva based oral cancer screening and prognosis tests may lead to better treatment options.

scholarly journals Poorly Differentiated Small-Cell-Type Neuroendocrine Carcinoma of the Prostate: A Case Report and Literature Review

2018 ◽  
Vol 11 (3) ◽  
pp. 676-681 ◽  
Author(s):  
Kishore Kumar ◽  
Rafeeq Ahmed ◽  
Chime Chukwunonso ◽  
Hassan Tariq ◽  
Masooma Niazi ◽  
...  
Keyword(s):  
Neuroendocrine Tumors ◽  
Tumor Grade ◽  
Small Cell ◽  
The Body ◽  
Neuroendocrine Cells ◽  
Cell Type ◽  
Variable Response ◽  
Ki 67 ◽  
Platinum Based Chemotherapy ◽  
Poorly Differentiated

Neuroendocrine cells are widespread throughout the body and can give rise of neuroendocrine tumors due to abnormal growth of the chromaffin cells. Neuroendocrine tumors divide into many subtypes based on tumor grade (Ki-67 index and mitotic count) and differentiation. These tumors can be further divided into secretory and nonsecretory types based on the production of peptide hormone by tumor cells. Poorly differentiated small-cell-type neuroendocrine tumors are one of the subtypes of neuroendocrine tumors. These tumors are less common; however, they tend to be locally invasive and aggressive in behavior with poor overall median survival. Treatment of the nonsecretory small-cell type is modeled to small-cell lung cancer with a regimen consisting of platinum-based chemotherapy and etoposide with variable response. Here, we present a case of poorly differentiated small-cell neuroendocrine tumor originating from the prostate.

scholarly journals Crosstalk between cancer cells and blood endothelial and lymphatic endothelial cells in tumour and organ microenvironment

2015 ◽  
Vol 17 ◽  
Author(s):  
Esak Lee ◽  
Niranjan B. Pandey ◽  
Aleksander S. Popel
Keyword(s):  
Endothelial Cells ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Tumour Growth ◽  
Tumour Progression ◽  
Lymphatic Vessels ◽  
Cell Types ◽  
Malignant Cell ◽  
Lymphatic Endothelial Cells ◽  
Tumour Blood

Tumour and organ microenvironments are crucial for cancer progression and metastasis. Crosstalk between multiple non-malignant cell types in the microenvironments and cancer cells promotes tumour growth and metastasis. Blood and lymphatic endothelial cells (BEC and LEC) are two of the components in the microenvironments. Tumour blood vessels (BV), comprising BEC, serve as conduits for blood supply into the tumour, and are important for tumour growth as well as haematogenous tumour dissemination. Lymphatic vessels (LV), comprising LEC, which are relatively leaky compared with BV, are essential for lymphogenous tumour dissemination. In addition to describing the conventional roles of the BV and LV, we also discuss newly emerging roles of these endothelial cells: their crosstalk with cancer cells via molecules secreted by the BEC and LEC (also called angiocrine and lymphangiocrine factors). This review suggests that BEC and LEC in various microenvironments can be orchestrators of tumour progression and proposes new mechanism-based strategies to discover new therapies to supplement conventional anti-angiogenic and anti-lymphangiogenic therapies.

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