Atherosclerosis is an inflammatory disease. Because high plasma concentrations of cholesterol, in particular those of low-density lipoprotein (LDL) cholesterol, are one of the principal risk factors for atherosclerosis,1 the process of atherogenesis has been considered by many to consist largely of the accumulation of lipids within the artery wall; however, it is much more than that. Despite changes in lifestyle and the use of new pharmacologic approaches to lower plasma cholesterol concentrations,2,3 cardiovascular disease continues to be the principal cause of death in the United States, Europe, and much of Asia.4,5 In fact, the lesions of atherosclerosis represent . . .

https://www.nejm.org/doi/pdf/10.1056/NEJM199901143400207

Atherosclerosis — An Inflammatory Disease

Atherosclerosis is an Inflammatory Disease

Dentinal repair in the postnatal organism occurs through the activity of specialized cells, odontoblasts, that are thought to be maintained by an as yet undefined precursor population associated with pulp tissue. In this study, we isolated a clonogenic, rapidly proliferative population of cells from adult human dental pulp. These DPSCs were then compared with human bone marrow stromal cells (BMSCs), known precursors of osteoblasts. Although they share a similar immunophenotype in vitro, functional studies showed that DPSCs produced only sporadic, but densely calcified nodules, and did not form adipocytes, whereas BMSCs routinely calcified throughout the adherent cell layer with clusters of lipid-laden adipocytes. When DPSCs were transplanted into immunocompromised mice, they generated a dentin-like structure lined with human odontoblast-like cells that surrounded a pulp-like interstitial tissue. In contrast, BMSCs formed lamellar bone containing osteocytes and surface-lining osteoblasts, surrounding a fibrous vascular tissue with active hematopoiesis and adipocytes. This study isolates postnatal human DPSCs that have the ability to form a dentin/pulp-like complex.

/pdf/postnatal-human-dental-pulp-stem-cells-dpscs-in-vitro-and-in-120dw1g1sy.pdf

Postnatal human dental pulp stem cells (DPSCs) in vitro and in vivo

https://www.exphem.org/article/S0301-472X(00)00482-3/pdf

Mesenchymal stem cells: Biology and potential clinical uses

Extracellular matrix structure.

Characterization of human bone marrow stromal cells with respect to osteoblastic differentiation

An increased plasma homocysteine level is an independent risk factor for vascular disease. However, the pathological mechanisms by which homocysteine promotes atherosclerosis are not yet clearly defined. Arterial smooth muscle cells cultured in the presence of homocysteine grew to a higher density and produced and accumulated collagen at levels significantly above control values. Homocysteine concentrations as low as 50 mumol/L significantly increased both cell density and collagen production. Cell density increased by as much as 43% in homocysteine-treated cultures. Homocysteine increased collagen production in a dose-dependent manner. Smooth muscle cells treated with homocysteine at concentrations observed in patients with hyperhomocysteinemia had collagen synthesis rates as high as 214% of control values. Likewise, collagen accumulation in the cell layer was nearly doubled in homocysteine-treated cultures. Addition of aquacobalamin to homocysteine-treated cultures controlled the increase in smooth muscle cell proliferation and collagen production. These results indicate a cellular mechanism for the atherogenicity of homocysteine and provide insight into a potential preventive treatment.

Homocysteine as a Risk Factor for Vascular Disease: Enhanced Collagen Production and Accumulation by Smooth Muscle Cells

Intracellular hyaluronan: a new frontier for inflammation?

https://www.jbc.org/content/276/32/30111.full.pdf

Alana K. Majors

Papers

Characterization of human bone marrow stromal cells with respect to osteoblastic differentiation

Homocysteine as a Risk Factor for Vascular Disease: Enhanced Collagen Production and Accumulation by Smooth Muscle Cells

Intracellular hyaluronan: a new frontier for inflammation?

Albumin thiolate anion is an intermediate in the formation of albumin-S-S-homocysteine

Endoplasmic Reticulum Stress Induces Hyaluronan Deposition and Leukocyte Adhesion