About

Rejji Kuruvilla is a professor of biology at Johns Hopkins University, serving as Vice Dean for Natural Sciences. Her research focuses on the development and functions of the sympathetic nervous system, a key regulator of whole-body physiology. Her laboratory studies how peripheral organs instruct sympathetic neuron development through mechanisms regulating neuron survival, axon growth, and target innervation. Her work has identified molecular and cellular mechanisms, such as axonal transport of neurotrophin receptors, that influence sympathetic neuron development and function. She has also investigated the role of sympathetic innervation in organ development, particularly in pancreatic islets, and how sympathetic dysfunction underlies pathologies like peripheral neuropathies, heart failure, hypertension, and diabetes. Additionally, her research explores the influence of satellite glial cells on sympathetic neurons, revealing their role in modulating sympathetic activity and implications for cardiovascular health.

Research topics

• Biology
• Neuroscience
• Cell biology
• Endocrinology
• Physics
• Genetics

Selected publications

• Transcytosis-mediated anterograde transport of the receptor TrkA mediates the formation of presynaptic sites in sympathetic neurons

  Science Signaling · 2026-05-12

  articleSenior authorCorresponding

  In neurons, many membrane proteins that are synthesized in the cell body must be efficiently delivered to axons to regulate neuronal connectivity. Transcytosis is an atypical transport mode in which membrane proteins internalized from soma membranes are transported to axons in an anterograde fashion. Here, we characterized the trafficking dynamics and mechanism of transcytosis of the receptor TrkA from the soma in response to nerve growth factor (NFG) signaling at the axon in mouse sympathetic neurons. Live imaging and electron microscopy of compartmentalized cultures revealed that soma surface-derived TrkA proteins underwent dynamic transport in axons, with changes in speed, direction, and the vesicular organelles that carried them as they moved from proximal to distal axon compartments. In mice, soma surface-labeled TrkA proteins were observed in sympathetic nerve terminals, demonstrating that transcytosis occurs in vivo. Transcytosed TrkA proteins were enriched at presynaptic varicosities, bouton-like structures that store and release neurotransmitters. Disrupting its transcytosis by introducing a point mutation into TrkA reduced the number and size of presynaptic sites and decreased synaptic transmission in vivo and in culture. These findings provide mechanistic insight into an atypical mode of receptor trafficking and demonstrate its physiological relevance in sympathetic neuron connectivity in mice.

  PublisherDOI

• Retrograde control of sympathetic neuron-satellite glia interactions by target-derived NGF signaling

  Cell Reports · 2025-12-01 · 1 citations

  articleOpen accessSenior author

  Satellite glial cells (SGCs) are the major glial cells in sympathetic ganglia contacting neuronal cell bodies. The intimate association of SGCs with sympathetic neurons ideally positions these glia as critical regulators of neuronal homeostasis, architecture, and function. However, how these neuron-glia interactions are established remains unclear. Here, we find a contact-mediated pathway triggered by retrograde signaling from innervated sympathetic targets that underlies neuron-SGC interactions, neuronal morphology, and functional output. We show that neuronal expression of a transmembrane protein, Delta/Notch-like EGF-related receptor (DNER), is dependent on signaling by target-derived nerve growth factor (NGF). Neuronal DNER deletion disrupts neuron-SGC contacts and results in aberrant neuronal morphology, including decreased soma size and hyper-innervation of targets in mice. DNER mutant neurons have elevated activity, and mice lacking neuronal DNER exhibit increased heart rate and thermogenesis, indicative of enhanced sympathetic tone. These results suggest a mechanism whereby innervated targets control assembly of functional neuron-glia units in the sympathetic nervous system.

  PublisherDOI

• Transcytosis-mediated anterograde transport of TrkA receptors controls formation of presynaptic sites in sympathetic neurons

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-09-21

  preprintOpen accessSenior authorCorresponding

  Abstract In neurons, many membrane proteins, synthesized in cell bodies, must be efficiently delivered to axons to influence neuronal connectivity. Transcytosis is an atypical transport mode, where membrane proteins internalized from soma surfaces are anterogradely transported to axons. Here, we define the trafficking dynamics and the transport vesicles involved in transcytosis of TrkA neurotrophin receptors and demonstrate that transcytosis controls formation of presynaptic sites in sympathetic neurons. Live imaging and electron microscopy in compartmentalized cultures revealed that soma surface-derived TrkA receptors undergo dynamic movements in axons and are housed in endosomes and multi-vesicular bodies. Soma-surface labeled TrkA appear in nerve terminals, demonstrating transcytosis occurs in vivo . Notably, transcytosed TrkA receptors are enriched at presynaptic varicosities. Disruption of transcytosis impairs the number and morphology of presynaptic sites and decreases synaptic transmission. These findings provide mechanistic insight into an atypical mode of receptor trafficking and highlights its physiological relevance in sympathetic neuron connectivity.

  PublisherDOI

• Satellite glial cells: Shaping peripheral input into the brain-body axis?

  Neuron · 2025-07-02 · 7 citations

  reviewOpen access
  PublisherOA PDFDOI

• Light modulates glucose and lipid homeostasis via the sympathetic nervous system

  Science Advances · 2024-12-11 · 7 citations

  articleOpen accessCorresponding

  Light is an important environmental factor for vision and for diverse physiological and psychological functions. Light can also modulate glucose metabolism. Here, we show that in mice, light is critical for glucose and lipid homeostasis by regulating the sympathetic nervous system, independent of circadian disruption. Light deprivation from birth elicits insulin hypersecretion, glucagon hyposecretion, lower gluconeogenesis, and reduced lipolysis by 6 to 8 weeks in male, but not female, mice. These metabolic defects are consistent with blunted sympathetic activity, and indeed, sympathetic responses to a cold stimulus are substantially attenuated in dark-reared mice. Further, long-term dark rearing leads to body weight gain, insulin resistance, and glucose intolerance. Notably, metabolic dysfunction can be partially alleviated by 5 weeks exposure to a regular light-dark cycle. These studies provide insight into circadian-independent mechanisms by which light directly influences whole-body physiology and better understanding of metabolic disorders linked to aberrant environmental light conditions.

  PublisherDOI

• Light modulates glucose and lipid homeostasis via the sympathetic nervous system

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-10-12

  preprintOpen access

  Light is an important environmental factor for vision, and for diverse physiological and psychological functions. Light can also modulate glucose metabolism. Here, we show that in mice, light is critical for glucose and lipid homeostasis by regulating the sympathetic nervous system, independent of circadian disruption. Light deprivation from birth elicits insulin hypersecretion, glucagon hyposecretion, lower gluconeogenesis, and reduced lipolysis by 6-8 weeks, in male, but not, female mice. These metabolic defects are consistent with blunted sympathetic activity, and indeed, sympathetic responses to a cold stimulus are significantly attenuated in dark-reared mice. Further, long-term dark rearing leads to body weight gain, insulin resistance, and glucose intolerance. Notably, metabolic dysfunction can be partially alleviated by 5 weeks exposure to a regular light-dark cycle. These studies provide insight into circadian-independent mechanisms by which light directly influences whole-body physiology and inform new approaches for understanding metabolic disorders linked to aberrant environmental light conditions.

  PublisherOA PDFDOI

• Sympathetic NPY controls glucose homeostasis, cold tolerance, and cardiovascular functions in mice

  Cell Reports · 2024-01-21 · 26 citations

  articleOpen accessSenior authorCorresponding

  Neuropeptide Y (NPY) is best known for its effects in the brain as an orexigenic and anxiolytic agent and in reducing energy expenditure. NPY is also co-expressed with norepinephrine (NE) in sympathetic neurons. Although NPY is generally considered to modulate noradrenergic responses, its specific roles in autonomic physiology remain under-appreciated. Here, we show that sympathetic-derived NPY is essential for metabolic and cardiovascular regulation in mice. NPY and NE are co-expressed in 90% of prevertebral sympathetic neurons and only 43% of paravertebral neurons. NPY-expressing neurons primarily innervate blood vessels in peripheral organs. Sympathetic-specific NPY deletion elicits pronounced metabolic and cardiovascular defects in mice, including reductions in insulin secretion, glucose tolerance, cold tolerance, and pupil size and elevated heart rate, while notably, however, basal blood pressure was unchanged. These findings provide insight into target tissue-specific functions of NPY derived from sympathetic neurons and imply its potential involvement in metabolic and cardiovascular diseases.

  PublisherOA PDFDOI

• Sympathetic NPY controls glucose homeostasis, cold tolerance, and cardiovascular functions in mice

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-07-26 · 3 citations

  preprintOpen accessSenior authorCorresponding

  Neuropeptide Y (NPY) is best known for its effects in the brain as an orexigenic and anxiolytic agent and in reducing energy expenditure. NPY is also co-expressed with Norepinephrine (NE) in sympathetic neurons. Although NPY is generally considered to modulate noradrenergic responses, its specific roles in autonomic physiology remain under-appreciated. Here, we show that sympathetic-derived NPY is essential for metabolic and cardiovascular regulation in mice. NPY and NE are co-expressed in 90% of prevertebral sympathetic neurons and only 43% of paravertebral neurons. NPY-expressing neurons primarily innervate blood vessels in peripheral organs. Sympathetic-specific deletion of NPY elicits pronounced metabolic and cardiovascular defects in mice, including reductions in insulin secretion, glucose tolerance, cold tolerance, pupil size, and an elevation in heart rate, while notably, however, basal blood pressure was unchanged. These findings provide new knowledge about target tissue-specific functions of NPY derived from sympathetic neurons and imply its potential involvement in metabolic and cardiovascular diseases.

  PublisherOA PDFDOI

• Supplementary Figure 3 from Myeloid-Derived Suppressor Cells Are a Major Source of Wnt5A in the Melanoma Microenvironment and Depend on Wnt5A for Full Suppressive Activity

  2023-03-31

  preprintOpen access

  <p>Supplementary Figure 3 - Effects of Myeloid Wnt5A Knockdown on Apoptosis, and Wnt5A Expression in Cell lines and Tumor Lysates</p>

  PublisherOA PDFDOI

• Supplementary Fig 1 from Myeloid-Derived Suppressor Cells Are a Major Source of Wnt5A in the Melanoma Microenvironment and Depend on Wnt5A for Full Suppressive Activity

  2023-03-31

  preprintOpen access

  <p>upplementary Figure 1 - Wnt5A Decreases Proliferation Specifically in Tumors Via the Recruitment of MDSCs</p>

  PublisherDOI

Recent grants

• NIH Grant R01NS073751

  NIH · $1.7M · 2017

• Neurotrophins as new regulators of islet biology

  NIH · $1.4M · 2015–2019

• Neurotrophic factor trafficking and signaling in development and disease

  NIH · $1.7M · 2019–2024

• NIH Grant R21DK090624

  NIH · $444k · 2013

• Coupled axonal protein synthesis and lipidation in axon growth and homeostasis

  NIH · $2.2M · 2019–2025

Frequent coauthors

• David D. Ginty

  Harvard University

  23 shared

• Mitchell E. Fane

  19 shared

• Ashani T. Weeraratna

  19 shared

• Yash Chhabra

  19 shared

• Stephen M. Douglass

  Connecticut College

  19 shared

• Xiangfan Yin

  17 shared

• Curtis H. Kugel

  17 shared

• Dmitry I. Gabrilovich

  17 shared

Labs

• Kuruvilla LabPI

Education

• Post-doctoral fellow, Neuroscience

  Johns Hopkins School of Medicine

  2005

• PhD, Biochemistry

  University of Houston

  1998