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Cell Behavior & Wound Healing

To maintain epidermal integrity and homeostasis, proper cell-cell adhesion and communication are critical. For the epidermis to fulfill its primary protective function, the orderly complex process of differentiation, which results in the formation of the outermost stratum corneum must occur. To respond to wounding, the epidermis must undergo proliferation and migration. Several laboratories within the Department of Dermatology are investigating the roles of epidermal proteins and glycolipids in these biological processes and applying them to translational mouse models. The expertise in epidermal cell biology underlies Northwestern's Skin Biology & Diseases Resource-Based Center, one of six such NIH-funded centers in the U.S.

 Irina Budunova Lab

Studying the role of the glucocorticoid receptor in carcinogenesis  and stem cell maintenance. Involved in development GR-targeted therapies in skin.

Research Description

The current projects in Dr. Budunova’s lab are centered on the role of the glucocorticoid receptor (GR) as a tumor suppressor gene in skin. We showed that skin-specific GR transgenic animals are resistant to skin carcinogenesis and GR KO animals are more sensitive to skin tumor development.  We are also interested in the role of GR in the maintenance of skin stem cells (SC). We found that GR/glucocorticoids inhibit the expression of numerous SC markers in skin including CD34- a marker of hair follicular epithelial SC and reduce the proliferative potential of skin SCs.

The glucocorticoids remain among the most effective and frequently used anti-inflammatory drugs in dermatology. Unfortunately, patients chronically treated with topical glucocorticoids, develop side effects including cutaneous atrophy. GR controls gene expression via (i) transactivation that requires GR dimerization and binding as homo-dimer to gene promoters and (ii) transrepression that is chiefly mediated via negative interaction between GR and other transcription factors including pro-inflammatory factor NF-kB. In general, GR transrepression is the leading mechanism of glucocorticoid anti-inflammatory effects, while many adverse effects of glucocorticoids are driven by GR transactivation.

Our laboratory has been involved in delineation of mechanisms underlying side effects of glucocorticoids in skin. Using GRdim knockin mice characterized by impaired GR dimerization and activation, we found that GR transactivation plays an important role in skin atrophy. These data suggested that non-steroidal selective GR activators (SEGRA) that do not support GR dimerization, could preserve therapeutic potential of classical glucocorticoids but have reduced adverse effects in skin.  We are testing effects of the novel SEGRA called Compound A– a synthetic analog of natural aziridine precursor from African bush Salsola Botch in skin. We have also established anti-cancer GR-dependent activity of Compound A in epithelial and lymphoma cells.

Using knockout mice for the major GR target genes including Fkbp5 (GR chaperone) and DDIT4/REDD1 (one of the major negative regulators  of mTORC), we discovered that blockage of Fkbp5 and REDD1 significantly changes GR function and greatly protects skin against glucocorticoid-induced atrophy. This suggests a novel GR-targeted anti-inflammatory therapy where glucocorticoids are combined with inhibitors of GR target genes.

For more information, please see Dr. Budunova’s faculty profile.


See Dr. Budunova's publications in PubMed.

Contact Budunova Lab

Contact the Budunova Lab at 312-503-4669 or visit in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 9-015, Chicago, IL 60611


Irina Budunova, MD, PhD

Research Associates

Pankaj Bhalla, PhDGleb Baida, PhDAnna Klopot, PhD

 Robert Lavker Lab

Investigating the biology of epithelial stem cells and how stem cells are regulated by microRNAs.

Research Description

The Lavker laboratory focuses on the biology of epithelial stem cells and the roles of microRNAs (miRNAs) in regulating epithelial homeostasis. In collaboration with Tung-Tien Sun (NYU Medical School), the lab identified and characterized stem cells of the epidermis, hair follicle and corneal epithelium. We have demonstrated that the hair follicle stem cells (located in the bulge region of the follicle) are pluripotent; capable of forming the hair shaft as well as the epidermis. Collectively, these studies have been of major importance for their implications regarding tissue regeneration, hair follicle growth, and carcinogenesis.

Initial investigations on microRNAs (miRNAs) focused on corneal epithelial-preferred miRNAs. Specifically, miR-205 undergoes a unique form of regulation through an interaction with the corneal-preferred miR-184 to maintain SHIP2 levels. SHIP2, a lipid phosphatase, is a target of miR-205, which enhances keratinocyte survival through PI3K-Akt signaling. This miRNA also positively regulates keratinocyte migration by altering F-actin organization and decreasing cell-substrate adhesion.

Recently, the lab has focused on miR-31, which targets factor inhibiting hypoxia-inducible factor-1 (FIH-1). FIH-1 impairs epithelial differentiation via attenuation of Notch signaling. Our results define a previously unknown mechanism for keratinocyte fate decisions where Notch signaling potential is, in part, controlled through a miR-31/FIH-1 nexus. This provides a rationale for development of treatment regimens in patients with diseases affecting abnormal epithelial differentiation (e.g., psoriasis) using inhibitors of FIH-1.

We have also demonstrated that miR-31 targets FIH-1 to positively regulate corneal epithelial glycogen metabolism, which results in the accumulation of glycogen. Increased glucose in the form of glycogen may be a mechanism by which the corneal epithelium is able to withstand periods of hypoxia during eyelid closure or extended contact lens wear. Thus miR-31 may function as a novel means if protecting the corneal epithelium from hypoxic stress.

Most recently, the laboratory has defined the microRNA expression patterns of the stem cell-enriched limbal basal cells and has begun to identify targets that are unique to the limbal epithelium. This should lead to an understanding of how miRNAs regulate epithelial stem cells.


For publication information and more, see the Lab faculty’s profiles:

Robert Lavker, PhDHan Peng, PhD

Contact Lavker Lab

Contact the Lavker Lab at 312-503-2043 or visit us on campus in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 9-120, Chicago, Illinois, 60611.


Robert M. Lavker, PhD, Han Peng, PhD

Postdoctoral Fellows

Nihal Kaplan, PhD


Wending Yang, PhD

Visiting Scholar

Junyi Wang, PhD

 Kurt Lu Lab
The focus of the lab is to better understand and control inflammation in the skin with goals of translating the findings into therapeutics for wound healing.  The lab has repurposed drugs such as vitamin D3 to control macrophage activation for repair of the skin following chemical exposure and UV-induced sunburns.  Using in vitro, animal models, and clinical trials, new compounds are being tested and developed towards these efforts.

Research Description

​The lab has a significant interest in elucidating how various drug compounds direct macrophage differentiation towards either an M1 classically activated vs. M2 alternatively activated phenotype, the latter being vital in tissue repair. The team has developed methods for repurposing drugs, such as the use of ultra-high doses of vitamin D3 in controlling innate immune activation in the skin. Recent discoveries from the lab demonstrate that vitamin D upregulates macrophage autophagy which is critical for the development of tissue repair M2 macrophages in the skin. The methodologies used in the lab spread the gamut from cell biology, to model organisms, to clinical trials.  ​The goal of the lab is to ultimately translate findings into the development of therapeutics for mediating skin and wound repair. This work has led to national and international recognition for the potential use of vitamin D3 and other immune-modifying drugs following skin injury in clinical scenarios such as UV sunburns and skin wounds from toxic chemical exposure.


For publication information and more, see Kurt Lu, MD

Contact Lu Lab

Contact the Lu Lab at 312-503-4075 or visit in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 4-202, Chicago, IL 60611


Kurt Lu, MD

Research Associates

Venus Onay, PhD; Dauren Biyashev, PhD

Research Technologists

Spencer Evans; Michael Demczuk

 Amy S. Paller Lab

a) Ganglioside modulation in diabetic wound healing and epidermal innervation abnormalities.

b) Impact of adiponectin on psoriasis severity and immunophenotype in obesity.

c) Utilizing siRNA and antisense Spherical Nucleic Acids (SNAs) to treat skin disorders.

Research Description

The Paller laboratory primarily focuses on inflammatory skin diseases and the development of novel therapeutic approaches. A long-term interest is the role in keratinocytes and other skin cells of lipid raft glycosphingolipids called gangliosides. The laboratory has shown that modulation of ganglioside content genetically (including by SNAs, see below) and biochemically profoundly affects skin cell function through affecting cell signaling. We have found that increases in membrane ganglioside expression suppress function of the epidermal growth factor receptor, insulin receptor, insulin-like growth factor receptor-1, and integrins, whereas depletion of ganglioside content stimulates receptor activation. The most recent translational research has involved use of ganglioside depletion using genetic and biochemical approaches to accelerate diabetic wound healing in human 3D and mouse diet-induced obese models, as well as to reverse the innervation abnormalities in back skin and footpads in diabetic models. 

A second area of interest is in immune abnormalities in psoriasis, with an emphasis on the impact of obesity. In both humans and mouse models, obesity increases the severity of psoriasis. The Paller laboratory has shown that the pro-inflammatory effect of obesity depends on reduction of adiponectin and that adiponectin mimetics reverse the tending towards psoriasis exacerbation through suppression of PPAR-gamma activation, reduction of Th17 skewing and increases in Treg cell activity.

Finally, an intense focus of investigation is topical application of siRNA and antisense spherical nucleic acids (SNAs) as a novel therapy for skin disorders. SNAs, in which the oligomers are densely arrayed around a central gold nanoparticle, were originally developed by the Mirkin laboratory at Northwestern. We have found that SNAs are: a) readily taken up into cultured keratinocytes; b) able to penetrate through the mouse and human epidermal barriers after application in a common moisturizer; c) suppress genes at nM to pM concentrations; d) have minimal off-target or immune effects after application; and e) to date, have shown no systemic or cutaneous toxicity. These studies have moved forward into showing improvement after topical application of SNAs directed against ganglioside GM3 synthase (diabetic wound healing), TNF or IL17RA or, using a bispecific, both targets (for psoriasis), and TGF-beta or CTGF for scars. SNAs for psoriasis have advanced to human trials.


For publication information and more, see Amy Paller's, MD/MS faculty profile.

Contact Paller Lab

Contact the Paller Lab at 312-503-0298 or visit us on campus in the Montgomery Ward Building at 303 E. Chicago Avenue, Ward 9-070, Chicago, Illinois, 60611.


Amy S. Paller, MD/MS

Senior Research Associate

Michael Bonkowski, PhD

Research Associate Professor

Xiao-Qi Wang, MD/PhD

Postdoctoral Fellows

Haoming Liu, PhD, Thomas Holmes, PhD

Visiting Predoctoral Fellow

Kevin Kwan


Kyle Dombeck

 Sergey Troyanovsky Lab

Investigating the mechanisms of adherens junctions assembly, dynamics and signaling.

The Troyanovsky lab’s research focuses on cadherin, intercellular adhesion and signaling. Classic cadherins are critical proteins mediating cell-cell adhesion and various signaling pathways responsible for cellular proliferation, differentiation and morphogenesis.  Abnormalities in this system are causal factors in many pathologies, including cancer. The molecular mechanisms of cadherin-based adhesion, however, are largely unknown. How do cadherins establish the adhesion contact? How do they interact with the cytoskeleton? What are the signaling pathways they control? Our laboratory's work is centered around these questions. We are currently working on the following specific projects:

  • An individual cadherin molecule’s adhesion site is very weak. To mediate tight adhesion, cadherin molecules form clusters. Recently our lab showed that cadherin clustering is based on two different mechanisms. First, using an extracellular cis-binding site, cadherin sticks laterally in small groups. Additional clustering is promoted by the actin cytoskeleton, binding to which limits cadherin diffusion. The aim of our current study is to understand the regulation of cadherin clustering through modulation of the cadherin-actin filament coupling.
  • The formation of cadherin adhesive clusters interconnected to the cytoskeleton is not sufficient to establish functional intercellular junctions. The junctions stimulate formation of actin bundles that is required for epithelial cells to organize their actin cytoskeleton. How adherens junctions initiate actin bundle formation is another direction in our research.
  • Cadherin is not the only transmembrane protein in adherens junctions. These structures contain adhesion proteins from the nectin family as well as numerous signaling proteins. We showed that one of such proteins, gamma-secretase, interacts with E-cadherin through p120-catenin. The roles of nectins and gamma-secretase and the ways they are recruited into adherens junctions are also areas of focus in our lab.

For more information see Sergey Troyanovsky’s, PhD, faculty profile.


View Dr. Troyanovsky's publications at PubMed.


Email Dr. Troyanovsky

Phone the Troyanovsky Lab at 312-503-9275

Lab Staff

Research Associates

Regina Troyanovsky, PhDIndrajyoti Indra, PhD

Postdoctoral Fellows

Mohammad Abu-Laban, PhD

 Bethany Perez White Lab

Investigating how epithelial cells communicate with one another through adhesion and signaling receptors.

Research Description

The Perez White laboratory strives to conduct leading-edge research in the field of epidermal biology with the ultimate goal of impacting medicine and advancing our understanding of skin. To this end, we incorporate hypothesis-driven research with innovative disease models and discovery approaches. Specifically, we employ three-dimensional models of bioengineered reconstituted human epidermis and mouse models with proteomics, RNA-sequencing, or microarray analysis. We uniquely exploit our use of primary human cells to identify key signal transduction mechanisms that drive the physiological state and how these pathways may be hijacked to contribute to pathological states.

The overall aim of our research direction is to define Eph receptor tyrosine kinase signal networks underlying epidermal homeostasis. As little is known about Eph receptors in skin biology, we performed a proteomics screen to generate a directory of EphA2-interacting proteins in primary human epidermal keratinocytes. So far, this rich resource has led us to appreciate an unrecognized role for EphA2 in tight junction morphogenesis. EphA2 promotes the de novo assembly and functional integrity of the epidermal tight junction barrier. The tight junction barrier is an indispensable structural network that prevents the movement of small molecules (water, solutes, ions, proteins, and pathogens, infectious agents, and allergens) into or out of an organism. Perturbations in tight junctions are relevant to several skin disorders such as cancer, atopic dermatitis, and psoriasis.


For more information, please see Dr. Perez White’s faculty profile.


See Dr. Perez White's publications in PubMed.

Contact Perez White Lab

Contact the Perez White Lab at 312-503-5452 or visit us on campus in the Montgomery Ward Building, 303 E. Chicago Avenue, Ward 9-321, Chicago, IL 60611.


Bethany Perez White, PhD

Research Associate

Ljuba Lyass, PhD

Postdoctoral Fellow

Nihal Kaplan, PhD


Shuangni Yang

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