Berry Lab

Key Findings

Adaptive Tissue Remodeling

Key Finding

Adaptive tissue remodeling progressively declines with aging. Our work demonstrated that aging impairs the recruitment of thermogenic beige adipocytes by disrupting the cellular mechanisms that support adaptive remodeling. These studies established that age-associated failure of adipose tissue adaptation reflects alterations within the tissue environment rather than an irreversible loss of adipogenic potential.

Representative publications

  1. Reversing Pdgfrβ signaling restores metabolically active beige adipocytes by alleviating ILC2 suppression in aged and obese mice.

  2. Age-dependent Pdgfrβ signaling drives adipocyte progenitor dysfunction to alter the beige adipogenic niche in male mice.

  3. Cellular Aging Contributes to Failure of Cold-Induced Beige Adipocyte Formation in Old Mice and Humans.

 

Progenitor Cell Biology

Key Finding

Adipose tissue contains specialized progenitor populations that perform distinct functions during tissue remodeling. Our studies identified molecular mechanisms that regulate adipocyte progenitor specification, maintenance, and lineage commitment during development and adulthood. These discoveries established adipocyte progenitors as dynamic regulators of tissue adaptation rather than passive precursor cells and revealed how alterations in progenitor biology influence adipose tissue growth and metabolic function.

Representative publications

  1. Cxcr4 regulates a pool of adipocyte progenitors and contributes to adiposity in a sex-dependent manner.

  2. Platelet-derived growth factor receptor beta is required for embryonic specification and confinement of the adult white adipose lineage.

  3. A PPARγ transcriptional cascade directs adipose progenitor cell-niche interaction and niche expansion.

  4. Independent stem cell lineages regulate adipose organogenesis and adipose homeostasis.

 

Cellular Niches

Key Finding

Specialized cellular niches regulate progenitor behavior and adaptive tissue remodeling. Our work demonstrated that progenitor function is governed by interactions with surrounding stromal, vascular, immune, and neural cell populations. These studies established that local niche organization actively regulates tissue remodeling and identified mechanisms through which disruption of niche function limits regenerative capacity and metabolic adaptation.

Representative publications

  1. Smooth muscle cell-derived Cxcl12 directs macrophage accrual and sympathetic innervation to control thermogenic adipose tissue.

  2. Macrophage-derived chemokine CCL22 establishes local LN-mediated adaptive thermogenesis and energy expenditure.

  3. Remodeling of gene regulatory networks underlying thermogenic stimuli-induced adipose beiging.

 

Intercellular Communication

Key Finding

Communication between stromal, immune, vascular, and neural cells coordinates adaptive tissue function. Our studies identified signaling pathways that coordinate interactions among multiple cellular populations to regulate thermogenesis, adipose remodeling, and metabolic homeostasis. These findings demonstrate that adaptive tissue function depends on integrated communication networks rather than the activity of individual cell types.

Representative publications

  1. PDGFRβ signaling restrains myocyte function to limit the regenerative capacity of skeletal muscle.

  2. Pyruvate Kinase M2 Supports Muscle Progenitor Cell Proliferation but Is Dispensable for Skeletal Muscle Regeneration after Injury.

  3. Smooth muscle cell-derived Cxcl12 directs macrophage accrual and sympathetic innervation to control thermogenic adipose tissue.