The bone marrow niche has mystified scientists for many years, leading to widespread investigation to shed light into its molecular and cellular composition. Considerable efforts have been devoted toward uncovering the regulatory mechanisms of hematopoietic stem cell (HSC) niche maintenance. Recent advances in imaging and genetic manipulation of mouse models have allowed the identification of distinct vascular niches that have been shown to orchestrate the balance between quiescence, proliferation and regeneration of the bone marrow after injury. Here we highlight the recently discovered intrinsic mechanisms, microenvironmental interactions and communication with surrounding cells involved in HSC regulation, during homeostasis and in regeneration after injury and discuss their implications for regenerative therapy.

/pdf/hematopoietic-stem-cell-niche-maintenance-during-homeostasis-3bdfmhipv8.pdf

Hematopoietic stem cell niche maintenance during homeostasis and regeneration

Stem cell ageing underlies the ageing of tissues, especially those with a high cellular turnover. There is growing evidence that the ageing of the immune system is initiated at the very top of the haematopoietic hierarchy and that the ageing of haematopoietic stem cells (HSCs) directly contributes to changes in the immune system, referred to as immunosenescence. In this Review, we summarize the phenotypes of ageing HSCs and discuss how the cell-intrinsic and cell-extrinsic mechanisms of HSC ageing might promote immunosenescence. Stem cell ageing has long been considered to be irreversible. However, recent findings indicate that several molecular pathways could be targeted to rejuvenate HSCs and thus to reverse some aspects of immunosenescence.

The ageing haematopoietic stem cell compartment

Cdc42 activity regulates hematopoietic stem cell aging and rejuvenation

Aging of hematopoietic stem cells (HSCs) is associated with a decline in their regenerative capacity and multilineage differentiation potential, contributing to the development of blood disorders. The bone marrow microenvironment has recently been suggested to influence HSC aging, but the underlying mechanisms remain largely unknown. Here we show that HSC aging critically depends on bone marrow innervation by the sympathetic nervous system (SNS), as loss of SNS nerves or adrenoreceptor β3 signaling in the bone marrow microenvironment of young mice led to premature HSC aging, as evidenced by appearance of HSC phenotypes reminiscent of physiological aging. Strikingly, supplementation of a sympathomimetic acting selectively on adrenoreceptor β3 to old mice significantly rejuvenated the in vivo function of aged HSCs, suggesting that the preservation or restitution of bone marrow SNS innervation during aging may hold the potential for new HSC rejuvenation strategies.

/pdf/adrenergic-nerve-degeneration-in-bone-marrow-drives-aging-of-569utelnn4.pdf

Adrenergic nerve degeneration in bone marrow drives aging of the hematopoietic stem cell niche.

In vitro analog of human bone marrow from 3D scaffolds with biomimetic inverted colloidal crystal geometry.

Hematopoietic stem cells (HSCs) from young and aged mice differ in their activity, and these differences in the activity are mostly intrinsic to HSCs. We therefore refer to aged HSCs and young HSCs when we speak of stem cells from aged and young animals. What are the molecular and cellular mechanisms that separate young HSCs from aged HSCs? Cell-cell interactions of HSCs with stroma cells in the stem cell niche are considered to be central for stem cell self-renewal as well as differentiation. We recently published data indicating that aged primitive hematopoietic cells are less adhesive to stroma cells when compared to young cells and that this altered interaction might be due to elevated activity of the small RhoGTPase Cdc42 in aged cells. In this manuscript we thus propose a novel model for stem cell aging: aged primitive hematopoietic cells are impaired in their ability to interact efficiently with stroma cells, which might result in the reduced self-renewal capacity as well as altered differentiation ability associated with aged stem cells.

Stem cells, aging, niche, adhesion and Cdc42: a model for changes in cell-cell interactions and hematopoietic stem cell aging.

Phase and porosity changes in a calcium aluminate cement and alumina system under hydrothermal conditions

Hematopoietic stem cells (HSCs) from young and aged mice differ in their activity, and these differences in the activity are mostly intrinsic to HSCs. We therefore refer to aged HSCs and young HSCs when we speak of stem cells from aged and young animals. What are the molecular and cellular mechanisms that separate young HSCs from aged HSCs?Cell‑cell interactions of HSCs with stroma cells in the stem cell niche are considered to be central for stem cell self‑renewal as well as differentiation. We recently published data indicating that aged primitive hematopoietic cells are less adhesive to stroma cells when compared to young cells and that this altered interaction might be due to elevated activity of the small RhoGTPase Cdc42 in aged cells. In this manuscript we thus propose a novel model for stem cell aging: aged primitive hematopoietic cells are impaired in their abil-ity to interact efficiently with stroma cells, which might result in the reduced self‑renewal capacity as well as altered differentiation ability associated with aged stem cells.

A Model for Changes in Cell-Cell Interactions and Hematopoietic Stem Cell Aging

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Stem cells, aging, niche, adhesion and Cdc42: a model for changes in cell-cell interactions and hematopoietic stem cell aging.

Phase and porosity changes in a calcium aluminate cement and alumina system under hydrothermal conditions

A Model for Changes in Cell-Cell Interactions and Hematopoietic Stem Cell Aging