bioRxiv Science⌕ Search

Biology subjects

Rothenbacher, D.

Publications and source records attributed to Rothenbacher, D..

2 recordsLinked to original sources

The extent of myeloid skewing in blood is a biomarker of biological aging in mice and humans

Myeloid skewing is a central and therefore often cited hallmark of hematopoietic aging. Myeloid skewing refers to an elevated myeloid-to-lymphoid cell ratio in aged compared to young mice. Interestingly, whether the extent of myeloid skewing might be in itself a quantitative biological marker of aging has not been addressed yet, nor whether this parameter has also relevance for the extent of aging in humans. Aged mice with high level of myeloid skewing (>50% myeloid cells in blood) showed accelerated hematopoietic aging compared to mice with a low level of myeloid skewing (<30% of myeloid cells in blood), as well as an increased level of inflammatory cytokines and elevated levels of diseases. Hematopoietic stem cells (HSCs) from mice with high myeloid skewing showed an impaired repopulation capacity. Epigenetic clock analyses demonstrated that mice with a high level of myeloid skewing present with a biological age that is older than their chronological age. In humans, a high degree of myeloid skewing was associated with elevated levels of inflammatory markers, reduced mobility, a greater burden of comorbidities, and an increased mortality hazard ratio. The data support that, besides overall myeloid skewing being a central hallmark of aging in mice, the extent of the frequency of myeloid cells in blood might serve as a biological marker of aging and disease in both mice and humans. Key PointsThe extent of myeloid skewing in aged mice correlates to an increased hematological and epigenetic age and increased disease burden. The extent of myeloid skewing in older adults is associated with an increased hazard ratio of mortality and correlates with higher frailty and inflammatory markers.

cell biology↗

p53-induced GDF-15 expression promotes a pro-regenerative response in human chondrocytes upon cartilage injury

Posttraumatic osteoarthritis (PTOA) is a special form of OA, developing after joint injuries. Except for some minor differences between the clinical characteristics of patients suffering from idiopathic OA (IOA) and PTOA, no biologic marker has yet been identified to distinguish IOA from PTOA. In this study, we investigated the expression of the stress-responsive cytokine growth differentiation factor 15 (GDF-15) in clinical samples from the Ulm OA study cohort (PTOA: n =12; IOA: n=54) and in a human ex vivo cartilage trauma model. We found significantly higher GDF-15 levels in synovial fluid of end-stage PTOA patients as compared to IOA patients. Further, we confirmed that fibroblast-like synoviocytes secreted increased levels of GDF-15 after stimulation with medium of ex vivo-traumatized cartilage. GDF-15 and its receptor, GFRAL, were significantly elevated in highly degenerated OA cartilage. By means of a human cartilage trauma model, we discovered that chondrocytes produced GDF-15 upon tissue injury, while antioxidative treatment attenuated GDF-15 secretion. We confirmed that oxidative stress and subsequent activation of p53 resulted in GDF-15 expression. As a transcriptional target of p53, GDF-15 was associated with chondrosenescence. Although the cytokine might therefore represent a senescence-associated secretory phenotype (SASP) factor, stimulation with exogenous GDF-15 did not cause detrimental effects but induced a pro-regenerative response in chondrocytes, characterized by enhanced proliferation as well as chondro- and cell protection after cartilage trauma. Overall, this study first describes GDF-15 as a stress-responsive and potentially pro-regenerative cytokine in the context of human PTOA.

cell biology↗